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The article provides a historical account of the Scandinavian involvement in the 'Zuntz-Chauveau controversy' regarding skeletal muscle fuel utilization during exercise. It discusses the research efforts of Scandinavian scientists, including Christensen, Nielsen, and Asmussen, and their contributions to understanding skeletal muscle metabolism. The controversy centered on whether carbohydrates are the exclusive substrate for muscle metabolism during exercise, with various scientists proposing different theories. The article highlights the challenges faced by researchers, such as dietary interventions and health issues, in conducting experiments to determine the role of carbohydrates and fats in muscle energy turnover. [Extracted from the article]

Background: This study focused on type 2 diabetes mellitus (T2DM) in a group of adult Mixe, an Indigenous population from Oaxaca, Mexico. Mixe comprised an estimated 9.4% (n ≅ 90 000) of the Indigenous population in Oaxaca. Mexico. Objective: This study focused on a group of adult Mixe, an Indigenous population from Oaxaca, Mexico. To compare the prevalence of T2DM, overweight (OW), obesity (OB), and hypertension (HTN) between 2007 and 2017 for a small, isolated Mixe community in the Valley of Oaxaca, Mexico. We test whether or not environmental changes have affected T2DM prevalence. Methods and Materials: Demographic and medical record data were collected in the community in 2007 and 2017 from the medical clinic and the mayor's office. T2DM was medically diagnosed among adults (>34 years old), in 2007 (n = 730) and in 2017 (n = 829). Results: T2DM crude prevalence increased from 6.7% to 12.1% (p <.001) from 2007 to 2017. The mean age of the sample analyzed was 60.6 (SD = 9.7). Age‐adjusted T2DM prevalence increased from 6.7% to 10.8% (p <.002). T2DM was 5.7%–5.5% among males (p <.53) and 7.1%–13.6% among females (p <.001). Sex‐specific OW and OB simulation studies indicate females had 7% less OW in 2007, and males were unchanged compared with 2017. OB among males and females was significantly higher in 2017 compared with 2007 (increased by 15.2% and 8.3%, males and females, respectively). Sexes combined OW + OB increased 12.7% among males but was unchanged in females (−0.5%). In the sexes combined analysis, OW prevalence increased 12.7% to 27.1% (p <.001) and OB prevalence increased 10.7%–27.9% (p <.001) from 2007 to 2017. HTN did not change significantly from 2007 to 2017 (15.4% and 14.6%, respectively) (p =.63) in adults. Among T2DM individuals, the frequency of HTN was not significantly different in 2007 and 2017 (57.1% and 37%, respectively) (p =.65). Transition to a Western diet consisting of high‐carbohydrate foods occurred at the same time as increased T2DM from 2007 to 2017, with a higher prevalence of T2DM noted among females in 2017. Conclusions: An increased prevalence of T2DM, OW, and OB but not HTN was observed in the Mixe community from 2007 to 2017 and was associated with the adoption of a high‐carbohydrate Western diet. [ABSTRACT FROM AUTHOR]

The present overview discusses the putative aphrodisiac properties of carbohydrates. It comprehensively investigates the intricate interplay between the physiological systems that govern sexual arousal and the consumption of carbohydrates in the diet. One method to achieve this is by examining the historical origins of aphrodisiacs in various civilizations. It highlights the significance of carbohydrates as essential macronutrients and explores their function in crucial biochemical processes associated with libido and sexual response. In order to understand the impact of dietary carbs on sexual health, the study examines the correlation among sex hormones, insulin sensitivity, and blood glucose levels. To understand how particular diets high in carbohydrates can improve sexual arousal, performance and desire the analysis looks at scientific research informing that some diets have aphrodisiac properties. The present research examines the influence of carbohydrates on mood, stress levels, and overall well‐being to gain a deeper understanding of the psychological underpinnings of sexual function. The points elucidated in this analysis enhance the understanding of the complex interrelationships between dietary components, specifically carbs, and sexual health. Results have implications for lifestyle modifications aimed at improving sexual well‐being. The information contained here will also be beneficial to individuals and healthcare professionals who are looking for evidence‐based approaches to improve their sexual well‐being. [ABSTRACT FROM AUTHOR]

South Asian immigrants in the United States face an elevated risk of developing type 2 diabetes (T2DM). This phenomenon has been linked to lifestyle factors and social determinants of health (SDOH) such as high-carbohydrate diet, limited physical activity, and stress from assimilation and other life challenges. Unfortunately, barriers stemming from language discordance, low health literacy, and certain cultural practices can hinder effective clinical management of T2DM among South Asian immigrants. In this perspective, we address these sociocultural barriers and propose culturally informed recommendations to improve healthcare delivery for South Asian groups and empower South Asian patients to self-manage T2DM. Our recommendations include (1) considerations and support for SDOH in South Asian communities, (2) culturally tailored healthcare delivery for South Asians, (3) mHealth technologies for T2DM education and self-management; and (4) enhanced epidemiological and South Asian-centric research. [ABSTRACT FROM AUTHOR]

This article discusses the perceptions, attitudes, and barriers to effective obesity care among people with obesity (PwO) and healthcare professionals (HCPs) in India. The study found that the majority of PwO and HCPs recognized obesity as a disease, but many PwO assumed self-responsibility for weight loss. Lack of exercise and unhealthy eating habits were identified as major barriers to weight loss. The study also highlighted the importance of initiating weight management discussions and addressing weight stigma. The authors suggest the need for a multidisciplinary approach and increasing awareness about obesity. [Extracted from the article]

Aim: Tirzepatide (Tzp), a novel dual agonist glucose‐dependent insulinotropic polypeptide/glucagon‐like peptide‐1, is approved for treating insulin resistance and obesity, and menopausal women consuming a high‐calorie diet are a target to study the Tzp effect. Therefore, we aimed to allometrically scale body weight (BW) in Tzp‐treated obese diabetic menopausal mice. Materials and Methods: Three‐month‐old C57BL/6 female mice had bilateral ovariectomy (Ovx) or a sham procedure and for 12 weeks were fed a control diet or a high‐fat and high sucrose diet (n = 120/each group [control (C), obese diabetic (Od), Ovx (O), sham (S), Tzp (T)]). Tzp was subcutaneously administered (10 nmol/kg) or vehicle once a day for an additional 4 weeks. The analysis considered log‐transformed data and the allometric equation log y = log a + b log x. Results: Od and OdO showed more upward slopes than C and CO. In C, BW was non‐allometric by T administration. Od and OdO showed slightly positive slopes (more prominent in OdO than Od). OdT and OdOT showed negative slopes, significant intercepts, and more robust Pearson coefficients than untreated ones. A potent drug effect was seen with BW allometric decline. Interactions between diet versus Ovx and diet versus Tzp affected weight gain. Diet versus Ovx versus Tzp affected food intake. Conclusions: A model was developed to show three usual factors observed in mature women. Notably, Tzp improved the metabolism and weight loss of OdO mice. Tzp‐treated mice showed negative allometric BW across treatment time, which is a quantitative assessment that allows better comparison between results. [ABSTRACT FROM AUTHOR]

Nutritional programming has the potential to enhance digestible carbohydrate utilization in fish; however, the underlying mechanisms remain unclear. The present study compared the metabolome, glucose metabolism-related gene expressions, and global DNA methylation between yellow catfish larvae, which were parental programmed by a high carbohydrate diet (HC) or not (CON). In total, 1509 differentially altered metabolites (DAMs) were identified. Among them, the contents of key intermediates of TCA cycle and pentose phosphate pathway, citrate, and D-glycero-L-galacto-octulose were higher in HC than in CON. Meanwhile, the contents of two epigenetic modification-related metabolites, 2-hydroxyglutaric acid and N1-acetylspermidine, differed significantly between HC and CON. Thirteen KEGG pathways were significantly enriched and were mainly linked to amino acid and lipid metabolism. Additionally, the pentose phosphate pathway was enriched. The mRNA expressions of glycolytic genes gk, pk, and pfk, as well as the glucose transport gene sglt1, were significantly higher in HC than in CON. Global DNA methylation was significantly higher in HC than in CON. These results suggested that high carbohydrate programming could improve glucose utilization in yellow catfish larvae by modulating the TCA cycle and pentose phosphate pathway, and enhancing the conversion of glucose to amino acids. Epigenetic modifications might be the underlying mechanisms by which nutritional programming affects glucose metabolism in fish, while 2-hydroxyglutaric acid and N1-acetylspermidine are two critical metabolites that mediate epigenetic modifications. [ABSTRACT FROM AUTHOR]

Background: Maternal obesity prepregnancy, as well as gestational overweight produced by high-sucrose diet, could be evolved to the cardiometabolic diseases in offspring during adulthood. Until then, the cardiometabolic diseases were ignored that have been presented or inherited in the offspring for overnutrition were ignored, depend on gender. We proposed that maternal prepregnancy obesity in CD1 mice, as well as gestational overweight produced by a high sucrose diet, develop to cardiometabolic disease in offspring and even if gender. For detection of the cardiometabolic diseases in a Murine model with a high sucrose diet (HSD), the time series formed by the RR intervals taken from lead I of the ECG has used the corresponding Poincare plot. The heart rate variability was characterized by the standard deviation of width and length SD1, SD2 respectively of the Poincare plot and the SD1/SD2 correlation index in addition was calculated between to gender and body weight. Results: A maternal diet was based high sucrose diet and produced overweight on progeny in both sexes, but the cardiac arrhythmias depended on gender. Other results were due to the chronic effect of high sucrose diet in offspring with this intrauterine ambiance that contributes to changes in HRV, arrhythmias, and sinus pauses, also these phenomena were observed just in the male mice offspring with high sucrose diet during adulthood. Conclusions: We propose, that the arrhythmias originated from fetal programming due to the maternal diet in mice model and produced alterations in the offspring female more than in the male, probably due to hormones. [ABSTRACT FROM AUTHOR]

Background: Astaxanthin (ASX) has been documented to exert beneficial influence on various processes in fish. Largemouth bass (Micropterus salmoides) serves as a common model for studying glucose-induced liver disease, making it imperative to investigate the regulatory mechanisms underlying its liver health. Methods: Largemouth bass were fed with a control diet (CON), a high carbohydrate diet (HC), or a HC diet supplemented astaxanthin (HCA) for 8-weeks, followed by the glucose tolerance test (GTT). Primary hepatocytes were treated with low glucose and high glucose combined with different concentrations of astaxanthin for 48 h. The histopathology, enzymology, transcriptomics, molecular biology and cell biology were combined to investigate the mechanism of liver injury. Results: This study provides evidence for the protective effects of ASX against growth performance reduction and hepatic liver injure in largemouth bass fed HC diet. In GTT, HCA diet exhibited an improvement in glucose tolerance following glucose loading. Although HCA diet did not restore the expression of insulin resistance-related genes in livers at different time during the GTT, the addition of ASX in the long-term HC diet did improve the insulin resistance pathway by regulating the PTP1B/PI3K/Akt signaling pathway. Hepatic transcriptome analyses showed that ASX plays an essential role in the modulation of glucose homeostasis in response to treated with HC diet. In in vitro study, ASX treatment resulted in an exaltation in cell viability and a reduction in the rate of cell apoptosis and reactive oxygen species (ROS). Additionally, astaxanthin was observed to improve apoptosis induced by high-glucose via p38MAPK/bcl-2/caspase-3 signaling pathway. Conclusions: Astaxanthin exhibited a protective effect against apoptosis by regulating p38MAPK/bcl-2/caspase-3 pathway, and ameliorated insulin resistance by activating the PTP1B/PI3K/Akt pathway. This study elucidated the mechanism of astaxanthin in the liver injury of largemouth bass from a new perspective and provided a new target for the treatment of insulin resistance. Highlights: ASX improved liver damage in diabetic largemouth bass. ASX improved apoptosis via p38MAPK/bcl-2/caspase-3 signaling pathway. ASX alleviated insulin resistance through the PTP1B/PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]

Summary Background Purpose Data sources Study selection Data extraction Data synthesis Limitations Conclusions Some dietary recommendations continue to recommend carbohydrate restriction as a cornerstone of dietary advice for people with diabetes.We compared the cardiometabolic effects of diets higher in both fiber and carbohydrate with lower carbohydrate lower fiber diets in type 1 or type 2 diabetes.MEDLINE, Embase, and the Cochrane Database of Systematic Reviews up to June 24, 2024, with additional hand searching.Randomized controlled trials in which both dietary fiber and carbohydrate amount had been modified were identified from source evidence syntheses on carbohydrate amount in people with diabetes.Two reviewers independently.Ten eligible trials including 499 participants with diabetes (98% with T2) were identified from the potentially eligible 828 trials included in existing evidence syntheses. Pooled findings indicate that higher fiber higher carbohydrate diets reduced HbA1c (mean difference [MD] −0.50% [95% confidence interval −0.99 to −0.02]), fasting insulin (MD −0.99 μIU/mL [−1.83 to −0.15]), total cholesterol (MD −0.16 mmol/L [−0.27 to −0.05]) and low‐density lipoprotein cholesterol (MD −0.16 mmol/L (−0.31 to −0.01) when compared with lower carbohydrate lower fiber diets. Trials with larger differences in fiber and carbohydrate intakes between interventions reported greater reductions. Certainty of evidence for these outcomes was moderate or high, with most outcomes downgraded due to heterogeneity unexplained by any single variable.Our predefined scope excluded trials with co‐interventions such as energy restriction, which may have provided addition information.Findings indicate the greater importance of promoting dietary fiber intakes, and the relative unimportance of carbohydrate amount in recommendations for people with diabetes. [ABSTRACT FROM AUTHOR]

Hyperglycaemia, hyperlipidaemia, hypertension and obesity are the main risk factors affecting the development and prognosis of ischaemic heart disease, which is still an important cause of death today. In our study, male Sprague–Dawley rats were fed either a standard diet (SD) or a high fat and high carbohydrate diet (HF‐HCD) for 8 weeks and streptozotocin (STZ) was injected at the seventh week of the feeding period. In one set of rats, a mixture of a prebiotic and probiotics (synbiotic, SYN) was administered by gavage starting from the beginning of the feeding period. Experimental myocardial ischaemia–reperfusion (30 min/60 min) was induced at the end of 8 weeks. Hyperglycaemia, hypertension and increased serum low‐density lipoprotein levels occurred in SD‐ and HF‐HCD‐fed and STZ‐treated rats followed for 8 weeks. Increased density of the Proteobacteria phylum was observed in rats with increased blood glucose levels, indicating intestinal dysbiosis. The severity of cardiac damage was highest in the dysbiotic HF‐HCD‐fed hyperglycaemic rats, which was evident with increased serum creatine kinase‐MB (CK‐MB), cardiac troponin I (cTnI), tumour necrosis factor‐α, and interleukin‐6 levels, along with a decrease in ST‐segment resolution index. SYN supplementation to either a normal or a high‐fat high‐carbohydrate diet improved gut dysbiosis, reduced anxiety, decreased CK‐MB and cTnI levels, and alleviated myocardial ischaemia–reperfusion injury in hyperglycaemic rats. [ABSTRACT FROM AUTHOR]

Introduction: Depression therapy has been linked to negative effects on energy metabolism, which can be attributed to various factors, including an ongoing inflammatory process commonly seen in metabolic disorders. Unhealthy lifestyle choices of patients and the impact of antidepressants on body weight and lipid and glucose metabolism also contribute to these metabolic side effects. Although not as pronounced as other psychopharmaceuticals, the increasing use of antidepressants raises concerns about their potential impact on public health. The study aimed to evaluate the short- and long-term effects of the antidepressant citalopram and its long-term combination with a special diet on metabolic parameters in mice. Methods: Animals were randomly divided into 5 groups – control, control + special diet, citalopram (10 mg/kg for 35 days), citalopram + special diet (10 mg/kg for 35 days), and citalopram (10 mg/kg for 7 days). After a described time of administration, animals were anesthetized, blood and fat and liver tissues were collected. Biochemical parameters of lipid metabolism (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides) and glucose were analyzed using spectrophotometry and relevant adipokines and cytokines were evaluated by ELISA. Results: After a week of application of citalopram, we observed dyslipidemia that persisted even at the end of the 5-week experiment. Furthermore, after 5 weeks of citalopram administration, we observed a significant decrease in body weight gain and decreased leptin levels. Changes in lipid metabolism, higher levels of adipokines leptin and PAI-1 were observed due to the special diet after 5 weeks. Conclusions: Our research suggests that the effects of citalopram and a diet on the metabolism of mice can be significant, both in the short term (1 week) and in the long term (5 weeks). [ABSTRACT FROM AUTHOR]

Poor nutrition is a risk factor for dental decay in younger people. However, except for sugar, it is unclear if this is true in older age groups. The aim of this study was to analyze the possible associations between overall dietary intake of nutrients and diet quality and the presence of dental decay in community-dwelling older men. A cross-sectional analysis of a longitudinal study with a standardized validated diet history assessment and comprehensive oral health examination in 520 community-dwelling men (mean age: 84 years) participating in the Concord Health and Ageing in Men Project. Nutrient reference values were used to determine if individual micronutrients and macronutrients were meeting recommendations. Acceptable macronutrient distribution ranges (AMDRs) were attained for fat and carbohydrate intakes and were incorporated into a dichotomous variable to determine if the participants were consuming a high fat-low carbohydrate diet. Diagnosis of coronal caries was based on visual criteria and inspection and was completed on each of the five coronal surfaces. Root surface caries was textual changes across four root surfaces. This diagnosis was used to categorize participants by the presence and severity of coronal and root caries. The adjusted logistic regression showed not meeting the recommended intakes for thiamin (odds ratio [OR]: 2.32 95% confidence interval [CI] 1.15–4.67), and zinc (OR: 3.33, 95% CI: 1.71–6.48) were associated with presence of severe root decay. Adjusted analysis also showed that participants who were outside the recommended AMDR for fat (OR: 0.61, 95% CI: 0.38–0.98) and those who consumed a high fat and low carbohydrate diet (OR: 0.56, 95% CI: 0.35–0.91) were less likely to have coronal tooth decay. Our study shows associations between micronutrients and macronutrients and coronal and root surface decay. Although this study cannot prescribe causality or be generalized to all older adults, diet has a possible association with dental decay in older men. [ABSTRACT FROM AUTHOR]

This study investigated the effects of curcumin nanoparticles on the flesh quality of largemouth bass on a high-carbohydrate diet. A total of 180 fish (11.01 ± 0.02 g) were fed three semi-purified diets: the Control group (LC) were supplemented with standard carbohydrate (10%), the experimental group (HC) were supplemented with 15% carbohydrate, and the experimental group were supplemented with 0.2% nano-curcumin added to 15% carbohydrate (HCN) for 6 weeks. Results showed that a* value, taurine, valine, isoleucine, histidine, cystine, fatty acids (C17:0 and C20:2n6), MDA (malondialdehyde) content, and SOD (Superoxide dismutase) activity were significantly elevated (p < 0.05) in HC. Muscle fibers showed significant increases in horizontal diameter, longitudinal diameter, and cross-sectional area (p < 0.05), as well as up-regulated expression levels of the MRFS (myogenic regulatory factor) family gene and MSTN (myostatin) (p < 0.05), and a significant decrease in C16:1n7 in HC (p < 0.05). Importantly, the HCN group enhanced the muscle quality of largemouth bass by elevating the L* value, valine, isoleucine, arginine and cystine, C20:2n6, decreasing (p < 0.05) refrigeration loss, chewability, firmness and hardness, then MDA content and SOD activity, and downregulating (p < 0.05) MSTN and MRFS family gene expression levels to improve largemouth bass muscle quality. [ABSTRACT FROM AUTHOR]

Background: The association between macronutrient consumption and the risk of type 2 diabetes (T2D) remains equivocal. Here, we investigated whether the quantity and quality of macronutrient intake are associated with T2D incidence in a West Asian population. Methods: T2D-free adults (n = 2457, mean age 38.5 ± 13.6 years, 54.2% women) who participated in the third examination cycle (2005–2008) of the Tehran Lipid and Glucose Study were followed for a median of 8.6 years. We estimated the macronutrient quality index (MQI), its individual sub-indices (carbohydrate quality index (CQI), fat quality index (FQI), and healthy plate protein quality index (HPPQI)), as well as the macronutrient quantity. The risk of T2D in relation to macronutrient quantity, quality, and their combined effects was examined using Cox proportional hazard models adjusted for known risk factors for T2D. Results: During the study follow-up, 257 incident cases of T2D were documented. Individuals in the highest tertiles of MQI and CQI had a 27% (HR = 0.73, 95% CI = 0.54, 0.98) and 29% (HR = 0.71, 95% CI = 0.51–0.99) lower T2D risk than those in the lowest tertiles. The T2D incidence was 35% lower in the middle HPPQI tertile than in the lowest (HR = 0.65, 95% CI = 0.47, 0.89). The multivariable adjusted model showed that individuals in the middle and highest tertiles of carbohydrate intake had 32% (HR = 0.68, 95% CI = 0.49–0.95) and 26% (HR = 0.74, 95% CI = 0.55–1.00) lower risks of T2D than individuals in the lowest tertile. A high-quantity, high-quality carbohydrate diet (≥ 58.5% of energy from carbohydrate with a CQI ≥ 13) and a low-glycemic index (GI), high-fiber diet (GI < 55 and fiber ≥ 25 g/d) were related to a reduced risk of T2D by 34% (HR = 0.66, 95% CI = 0.47, 0.93) and 42% (HR = 0.58, 95% CI = 0.38, 0.90), respectively. Conclusion: A diet with a higher carbohydrate quality may be associated with a lower T2D incidence, particularly when the carbohydrate quantity is also high. [ABSTRACT FROM AUTHOR]

Background: Existing data on maternal dietary patterns and birth weight remains limited and inconsistent, especially in non-Western populations. We aimed to examine the relationship between maternal dietary patterns and birth weight among a cohort of Chinese. Methods: In this study, 4,184 mother-child pairs were included from the Iodine Status in Pregnancy and Offspring Health Cohort. Maternal diet during pregnancy was evaluated using a self-administered food frequency questionnaire with 69 food items. Principal component analysis was used to identify dietary patterns. Information on birth weight and gestational age was obtained through medical records. Adverse outcomes of birth weight were defined according to standard clinical cutoffs, including low birth weight, macrosomia, small for gestational age, and large for gestational age. Results: Three maternal dietary patterns were identified: plant-based, animal-based, and processed food and beverage dietary patterns, which explained 23.7% variance in the diet. In the multivariate-adjusted model, women with higher adherence to the plant-based dietary patten had a significantly higher risk of macrosomia (middle tertile vs. low tertile: odds ratio (OR) 1.45, 95% CI 1.00-2.10; high tertile vs. low tertile: OR 1.55, 95% CI 1.03–2.34; P-trend = 0.039). For individual food groups, potato intake showed positive association with macrosomia (high tertile vs. low tertile: OR 1.72, 95% CI 1.20–2.47; P-trend = 0.002). Excluding potatoes from the plant-based dietary pattern attenuated its association with macrosomia risk. No significant associations was observed for the animal-based or processed food and beverage dietary pattern with birth weight outcomes. Conclusions: Adherence to a plant-based diet high in carbohydrate intake was associated with higher macrosomia risk among Chinese women. Future studies are required to replicate these findings and explore the potential mechanisms involved. [ABSTRACT FROM AUTHOR]

Sucrose intake is a potential risk factor for non-alcoholic fatty liver disease (NAFLD). Individual characteristics such as sex, play arole in the biological variation of the disease, potentially related to genetic regulation. This research evaluated sex differences in biochemical, histopathological, and gene expression responses associated with NAFLD in C57bl/6N mice on a high sucrose diet. Female and male mice were assigned to control or high sucrose diets (50% sucrose solution) for 20 weeks. After sacrifice, blood and hepatic tissue were collected for analysis. Female mice revealed moderate-to-high NAFLD, whereas male mice showed mild-to-moderate NAFLD. Sex-specific variations were observed in Cd36 gene expression, an upregulation in females compared with the male group, and Adipor1 gene expression showed significant downregulation in the female group in response to high sucrose diet compared with the control group. These findings highlight the importance of considering gender disparities in the treatment and management of NAFLD. [ABSTRACT FROM AUTHOR]

We studied the effect of a high-fat, high-carbohydrate diet (HFHCD) on basal testosterone levels in the blood and testosterone, its precursors, and expression of steroidogenic genes in the testes of rats treated with human chorionic gonadotropin (hCG, 10 IU/rat, subcutaneously, once), gonadotropin-releasing hormone receptor antagonist cetrorelix (75 μg/kg, subcutaneously, 3 days), and their combination. In HFHCD rats, no obvious signs of androgen deficiency were observed and the response of the testes to hCG stimulation was preserved. Unlike control rats (normal diet), the expression of the luteinizing hormone receptor gene in these rats did not change in response to hCG stimulation and cetrorelix administration; they also showed a paradoxical, more pronounced response to hCG administration under conditions of suppression of the gonadotropin secretion by cetrorelix. This suggests that the etiology and pathogenesis of obesity may have different effects on the hormonal status of the male reproductive system. [ABSTRACT FROM AUTHOR]

Background: Cognitive impairment is a prevalent complication of type 2 diabetes, influenced significantly by various dietary patterns. High-carbohydrate diets (HCDs) are commonly consumed nowadays; however, the specific impact of HCDs on cognitive function in diabetes remains unclear. Methods: The objective of this study was to investigate whether an HCD has effects on cognition in diabetes. Eight-week-old diabetic (db/db) mice and wild-type (WT) mice underwent a twelve-week dietary intervention, including a normal diet (ND), an HCD, or a high-fat diet (HFD). Following this, behavioral tests were conducted, and related hippocampal pathology was evaluated. Results: Our results demonstrated that an HCD exacerbated cognitive decline in db/db mice compared to an ND. Additionally, an HCD increased amyloid-β burden and expression of β-site APP cleaving enzyme-1. An HCD was also found to promote the phosphorylation of tau protein via the PI3K/Akt/GSK-3β pathway. Furthermore, an HCD markedly induced neuroinflammation and increased the quantity of microglia and astrocytes. However, these damages induced by an HCD were less severe than those caused by an HFD. Conclusions: Collectively, our findings indicate that a high intake of carbohydrates can have an adverse impact on cognitive function in diabetes. [ABSTRACT FROM AUTHOR]

High-fat and high-carbohydrate (HF-HC) diets induce metabolic syndrome via mitochondrial dysfunction and oxidative stress. We have previously shown that this may be prevented by avocado oil, a source of bioactive molecules with antioxidant properties. However, it is unknown if these effects are mediated by the unsaponifiable fraction of avocado oil (UFAO). Thus, we tested if this fraction improves glucose metabolism, bioenergetics and oxidative stress in mitochondria from the kidney and liver of rats fed an HF-HC diet. We found that 12 weeks of an HF-HC diet impaired glucose utilization and increased insulin resistance, which was prevented by UFAO administration. The HF-HC diet decreased respiration, membrane potential and electron transport chain (ETC) function in liver and kidney mitochondria. These mitochondrial dysfunctions were prevented by UFAO intake. Unexpectedly, UFAO increased ROS levels in the mitochondria of control animals and did not decrease them in rats with an HF-HC diet; however, UFAO protects liver and kidney mitochondria from iron-induced oxidative stress. These findings suggest that impairments in glucose metabolism and mitochondrial function by an HF-HC diet may be prevented by UFAO, without decreasing ROS generation but protecting mitochondria from oxidative damage. [ABSTRACT FROM AUTHOR]

To evaluate the effects of dietary supplementation with succinic acid on growth performance, flesh quality, glucose, and lipid metabolism of Nile tilapia (Oreochromis niloticus) fed a high-carbohydrate diet (HCD), five iso-nitrogenous and iso-lipidic diets were prepared as follows: HCD (control group) consisting of 55% corn starch and HCD supplemented with 0.5%, 1.0%, 2.0%, and 4.0% succinic acid, respectively. Tilapia with an initial body weight of 204.90 ± 1.23 g randomly assigned to 15 tanks with 3 replicates per group and 10 fish per tank fed for 8 weeks. Increasing dietary succinic acid supplementation resulted in significant second-order polynomial relationship in the weight gain rate (WGR), specific growth rate (SGR), feed conversion ratio (FCR), protein efficiency rate (PER), viscerosomatic index, condition factor, and contents of muscular crude lipid and glycogen (P

Cytochrome P450 2D (CYP2D) is important in psychopharmacology as it is engaged in the metabolism of drugs, neurosteroids and neurotransmitters. An unbalanced maternal diet during pregnancy and lactation can cause neurodevelopmental abnormalities and increases the offspring's predisposition to neuropsychiatric diseases. The aim of the present study was to evaluate the effect of maternal modified types of diet: a high-fat diet (HFD) and high-carbohydrate diet (HCD) during pregnancy and lactation on CYP2D in the liver and brain of male offspring at 28 (adolescent) or 63 postnatal days (young adult). The CYP2D activity and protein level were measured in the liver microsomes and the levels of mRNAs of CYP2D1, 2D2 and 2D4 were investigated both in the liver and brain. In the liver, both HFD and HCD increased the mRNA levels of all the three investigated CYP2D genes in adolescents, but an opposite effect was observed in young adults. The CYP2D protein level increased in adolescents but not in young adults. In contrast, young adults showed significantly decreased CYP2D activity. Similar effect of HFD on the CYP2D mRNAs was observed in the prefrontal cortex, while the effect of HCD was largely different than in the liver (the CYP2D2 expression was not affected, the CYP2D4 expression was decreased in young adults). In conclusion, modified maternal diets influence the expression of individual CYP2D1, CYP2D2 and CYP2D4 genes in the liver and brain of male offspring, which may affect the metabolism of CYP2D endogenous substrates and drugs and alter susceptibility to brain diseases and pharmacotherapy outcome. [ABSTRACT FROM AUTHOR]

AbstractThis work investigated the biochemical disturbances and histological alteration in Psammomys obesus animal model fed different high calorie diets (HCDs) during three months. Four diets were used: a low-calorie natural diet, Chenopodiaceae halophyte plant used as control (LCD), a high standard carbohydrate diet rich in protein, HCD 0, a high carbohydrate diet rich in two concentrations of fat, HCD 1 and HCD 2. All animals having received HCDs developed dyslipidemia after one month of experiment with distinction of different sub-groups developing or not obesity and diabetes. HCDs induced a remarkable increasing in blood cholesterol, LDL-cholesterol and triglyceride levels indicating a fast induction of dyslipidemia and a significant increase of aminotransaminases activities revealing a pronounced hepatotoxicity. Animal developing diabetes showed a severe hepatic injury, a degeneration of the adipose tissue and a significant reduction of retinal thickness. P. obesus seems to be an excellent animal model to investigate nutritional metabolic diseases. [ABSTRACT FROM AUTHOR]

Patients with sepsis experience metabolic and immunologic dysfunction that may be amplified by standard carbohydrate-based nutrition. A ketogenic diet (KD) may offer an immunologically advantageous alternative, although clinical evidence is limited. We conducted a single-center, open-label, randomized controlled trial to assess whether a KD could induce stable ketosis in critically ill patients with sepsis. Secondary outcomes included assessment of feasibility and safety of KD, as well as explorative analysis of clinical and immunological characteristics. Forty critically ill adults were randomized to either a ketogenic or standard high-carbohydrate diet. Stable ketosis was achieved in all KD patients, with significant increases in β-hydroxybutyrate levels compared with controls [mean difference 1.4 milimoles per liter; 95% confidence interval (CI): 1.0 to 1.8; P < 0.001). No major adverse events or harmful metabolic side effects (acidosis, dysglycemia, or dyslipidemia) were observed. After day 4, none of the patients in the KD group required insulin treatment, whereas in the control group, insulin dependency ranged between 35% and 60% (P = 0.009). There were no differences in 30-day survival, but ventilation-free [incidence rate ratio (IRR) 1.7; 95% CI: 1.5 to 2.1; P < 0.001], vasopressor-free (IRR 1.7; 95% CI: 1.5 to 2.0; P < 0.001), dialysis-free (IRR 1.5; 95% CI: 1.3 to 1.8; P < 0.001), and intensive care unit–free days (IRR 1.7; 95% CI: 1.4 to 2.1; P < 0.001) were higher in the ketogenic group. Next-generation sequencing of CD4+/CD8+ T cells and protein analyses showed reduced immune dysregulation, with decreased gene expression of T-cell activation and signaling markers and lower pro-inflammatory cytokine secretion. This trial demonstrated the safe induction of a stable ketogenic state in sepsis, warranting larger trials to investigate potential benefits in sepsis-related organ dysfunction. Editor's summary: Sepsis is characterized by immune dysregulation that may be worsened by metabolic dysfunction. A ketogenic diet may therefore be advantageous in the intensive care setting, where standard carbohydrate-based nutrition can worsen metabolic dysfunction. Here, Rahmel and colleagues conducted a single-center, open-label trial where 40 critically ill patients with sepsis were randomized to receive either a ketogenic diet or standard high-carbohydrate nutrition. Stable ketosis was successfully achieved in the patients receiving the ketogenic diet and was associated with improved clinical measures, although there were no differences in 30-day survival. Exploratory analyses also suggested reduced immune dysregulation in patients on the ketogenic diet. These results support further investigation of the effects of ketogenic diet on critically ill patients with sepsis. —Melissa L. Norton [ABSTRACT FROM AUTHOR]

We compared 2 models of metabolic syndrome in rats: high-fat diet (58% calories) with single streptozotocin injection at a dose of 25 mg/kg and replacement of water with 20% fructose solution. The model with fructose solution did not cause the main signs of metabolic syndrome over 24 weeks: concentrations of glucose, triglycerides, cholesterol, weight, and BP did not significantly differ from the control group (standard diet). At the same time, single streptozotocin administration was followed by the development of persistent hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and signs of visceral obesity. High-fat diet combined with injection of streptozotocin in a low dose can be considered a more representative model of metabolic syndrome in humans. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM) triggers alterations in the maternal microbiome. Alongside metabolic shifts, microbial products may impact clinical factors and influence pregnancy outcomes. We investigated maternal microbiome-metabolomic changes, including over 600 metabolites from a subset of the "Choosing Healthy Options in Carbohydrate Energy" (CHOICE) study. Women diagnosed with GDM were randomized to a diet higher in complex carbohydrates (CHOICE, n = 18, 60% complex carbohydrate/25% fat/15% protein) or a conventional GDM diet (CONV, n = 16, 40% carbohydrate/45% fat/15% protein). All meals were provided. Diets were eucaloric, and fiber content was similar. CHOICE was associated with increases in trimethylamine N-oxide, indoxyl sulfate, and several triglycerides, while CONV was associated with hippuric acid, betaine, and indole propionic acid, suggestive of a healthier metabolome. Conversely, the microbiome of CHOICE participants was enriched with carbohydrate metabolizing genes and beneficial taxa such as Bifidobacterium adolescentis, while CONV was associated with inflammatory pathways including antimicrobial resistance and lipopolysaccharide biosynthesis. We also identified latent metabolic groups not associated with diet: a metabolome associated with less of a decrease in fasting glucose, and another associated with relatively higher fasting triglycerides. Our results suggest that GDM diets produce specific microbial and metabolic responses during pregnancy, while host factors also play a role in triglycerides and glucose metabolism. [ABSTRACT FROM AUTHOR]

Consumption of a high-fat diet (HFD) has been suggested as a contributing factor behind increased intestinal permeability in obesity, leading to increased plasma levels of microbial endotoxins and, thereby, increased systemic inflammation. We and others have shown that HFD can induce jejunal expression of the ketogenic rate-limiting enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS). HMGCS is activated via the free fatty acid binding nuclear receptor PPAR-α, and it is a key enzyme in ketone body synthesis that was earlier believed to be expressed exclusively in the liver. The function of intestinal ketogenesis is unknown but has been described in suckling rats and mice pups, possibly in order to allow large molecules, such as immunoglobulins, to pass over the intestinal barrier. Therefore, we hypothesized that ketone bodies could regulate intestinal barrier function, e.g., via regulation of tight junction proteins. The primary aim was to compare the effects of HFD that can induce intestinal ketogenesis to an equicaloric carbohydrate diet on inflammatory responses, nutrition sensing, and intestinal permeability in human jejunal mucosa. Fifteen healthy volunteers receiving a 2-week HFD diet compared to a high-carbohydrate diet were compared. Blood samples and mixed meal tests were performed at the end of each dietary period to examine inflammation markers and postprandial endotoxemia. Jejunal biopsies were assessed for protein expression using Western blotting, immunohistochemistry, and morphometric characteristics of tight junctions by electron microscopy. Functional analyses of permeability and ketogenesis were performed in Caco-2 cells, mice, and human enteroids. Ussing chambers were used to analyze permeability. CRP and ALP values were within normal ranges and postprandial endotoxemia levels were low and did not differ between the two diets. The PPARα receptor was ketone body-dependently reduced after HFD. None of the tight junction proteins studied, nor the basal electrical parameters, were different between the two diets. However, the ketone body inhibitor hymeglusin increased resistance in mucosal biopsies. In addition, the tight junction protein claudin-3 was increased by ketone inhibition in human enteroids. The ketone body β-Hydroxybutyrate (βHB) did not, however, change the mucosal transition of the large-size molecular FD4-probe or LPS in Caco-2 and mouse experiments. We found that PPARα expression was inhibited by the ketone body βHB. As PPARα regulates HMGCS expression, the ketone bodies thus exert negative feedback signaling on their own production. Furthermore, ketone bodies were involved in the regulation of permeability on intestinal mucosal cells in vitro and ex vivo. We were not, however, able to reproduce these effects on intestinal permeability in vivo in humans when comparing two weeks of high-fat with high-carbohydrate diet in healthy volunteers. Further, neither the expression of inflammation markers nor the aggregate tight junction proteins were changed. Thus, it seems that not only HFD but also other factors are needed to permit increased intestinal permeability in vivo. This indicates that the healthy gut can adapt to extremes of macro-nutrients and increased levels of intestinally produced ketone bodies, at least during a shorter dietary challenge. [ABSTRACT FROM AUTHOR]

Background: Advanced glycation end product-modified low-density lipoprotein (AGE-LDL) is related to inflammation and the development of atherosclerosis. Additionally, it has been demonstrated that receptor for advanced glycation end products (RAGE) has a role in the condition known as calcific aortic valve disease (CAVD). Here, we hypothesized that the AGE-LDL/RAGE axis could also be involved in the pathophysiological mechanism of CAVD. Methods: Human aortic valve interstitial cells (HAVICs) were stimulated with AGE-LDL following pre-treatment with or without interleukin 37 (IL-37). Low-density lipoprotein receptor deletion (Ldlr−/−) hamsters were randomly allocated to chow diet (CD) group and high carbohydrate and high fat diet (HCHFD) group. Results: AGE-LDL levels were significantly elevated in patients with CAVD and in a hamster model of aortic valve calcification. Our in vitro data further demonstrated that AGE-LDL augmented the expression of intercellular cell adhesion molecule-1 (ICAM-1), interleukin-6 (IL-6) and alkaline phosphatase (ALP) in a dose-dependent manner through NF-κB activation, which was attenuated by nuclear factor kappa-B (NF-κB) inhibitor Bay11-7082. The expression of RAGE was augmented in calcified aortic valves, and knockdown of RAGE in HAVICs attenuated the AGE-LDL-induced inflammatory and osteogenic responses as well as NF-κB activation. IL-37 suppressed inflammatory and osteogenic responses and NF-κB activation in HAVICs. The vivo experiment also demonstrate that supplementation with IL-37 inhibited valvular inflammatory response and thereby suppressed valvular osteogenic activities. Conclusions: AGE-LDL promoted inflammatory responses and osteogenic differentiation through RAGE/NF-κB pathway in vitro and aortic valve lesions in vivo. IL-37 suppressed the AGE-LDL-induced inflammatory and osteogenic responses in vitro and attenuated aortic valve lesions in a hamster model of CAVD. [ABSTRACT FROM AUTHOR]

Background: Mounting evidence links glucose intolerance and diabetes as aspects of metabolic dysregulation that are associated with an increased risk of developing dementia. Inflammation and inflammasome activation have emerged as a potential link between these disparate pathologies. As diet is a key factor in both the development of metabolic disorders and inflammation, we hypothesize that long term changes in dietary factors can influence nervous system function by regulating inflammasome activity and that this phenotype would be sex-dependent, as sex hormones are known to regulate metabolism and immune processes. Methods: 5-week-old male and female transgenic mice expressing a caspase-1 bioluminescent reporter underwent cranial window surgeries and were fed control (65% complex carbohydrates, 15% fat), high glycemic index (65% carbohydrates from sucrose, 15% fat), or ketogenic (1% complex carbohydrates, 79% fat) diet from 6 to 26 weeks of age. Glucose regulation was assessed with a glucose tolerance test following a 4-h morning fast. Bioluminescence in the brain was quantified using IVIS in vivo imaging. Blood cytokine levels were measured using cytokine bead array. 16S ribosomal RNA gene amplicon sequencing of mouse feces was performed to assess alterations in the gut microbiome. Behavior associated with these dietary changes was also evaluated. Results: The ketogenic diet caused weight gain and glucose intolerance in both male and female mice. In male mice, the high glycemic diet led to increased caspase-1 biosensor activation over the course of the study, while in females the ketogenic diet drove an increase in biosensor activation compared to their respective controls. These changes correlated with an increase in inflammatory cytokines present in the serum of test mice and the emergence of anxiety-like behavior. The microbiome composition differed significantly between diets; however no significant link between diet, glucose tolerance, or caspase-1 signal was established. Conclusions: Our findings suggest that diet composition, specifically the source and quantity of carbohydrates, has sex-specific effects on inflammasome activation in the central nervous system and behavior. This phenotype manifested as increased anxiety in male mice, and future studies are needed to determine if this phenotype is linked to alterations in microbiome composition. [ABSTRACT FROM AUTHOR]

Introduction: Vascular calcification is a major cause of cardiovascular accidents in patients with type 2 diabetes mellitus. This study aimed to investigate the impact of carbohydrates on gut microbiota and aortic calcification in diabetic ApoE−/− mice. Methods: The diabetic ApoE−/− mice were randomly divided into 4 groups: ketogenic diet group, low carbohydrate diet group, medium carbohydrate diet group, and high carbohydrate diet group. The mice were fed continuously for 6 months, with blood glucose, blood ketone and body weight monitored monthly. Lipid metabolism indicators and inflammatory factors were detected using ELISA. The intestinal barrier, atherosclerotic lesion areas, and vascular calcifications were analyzed based on their morphology. Gut microbiota was analyzed using 16S rRNA genes. Results: We found that ketogenic diet played some roles improving glucose, lipid metabolism, and inflammation. Ketogenic diet could improve the intestinal barrier to some extent and increase intestinal bacteria. Compared to the other three groups, the relative abundance of genus Allobaculum, species Blautia producta and Clostridium Ramosum in the ketogenic diet group was significantly increased (P < 0.05), which has protective effects in diabetic ApoE−/− mice. Conclusion: Ketogenic diet could delay the onset of aortic atherosclerosis, aortic calcification and improve intestinal barrier function in diabetic ApoE−/− mice. [ABSTRACT FROM AUTHOR]

Background: Obesity and diabetes are interrelated growing problems worldwide. Life style modifications including nutritional intervention are considered the first line in management of diabetes. Materials and methods: Our study included 81 type 2 diabetic patients, all treated with Metformin 500 mg twice daily, with Body mass index (BMI) more than 25 kg/m2. They were randomized to one of three dietary interventions; high protein diet (Zone diet), high fat diet (Modified Atkins) and conventional high carbohydrates diet with consideration of being on a caloric deficit diet of 500 kcal per day. Patients were assessed by: body mass index, waist circumference and bioelectrical impedance analysis (BIA) method for assessment of body fat and muscle mass (FM, MM) before and after 12 weeks of following a dietary plan. Laboratory tests included: Hemoglobin A1c, C-reactive protein levels, lipid profile and insulin resistance before and after 12 weeks of following a dietary plan. Results: Significant weight loss and reduction of BMI, reduction of waist circumference, significant fat mass reduction, significant muscle mass reduction, improvement of the insulin resistance, LDL and triglyceride reduction was achieved by the three dietary plans, with no significant difference between them. There was also significant improvement in HbA1c in all dietary plans; however Modified Atkins diet showed more significant improvement. Significant HDL improvement was seen with High carbohydrate diet and Modified Atkins diet, with more significant reduction with Modified Atkins diet, while Zone diet did not show significant improvement. CRP marker of inflammation showed significant improvement with High carbohydrate diet and Modified Atkins diet, while Zone diet did not show significant improvement. Conclusion: All three dietary plans show benefit and improve the anthropometric and metabolic outcomes of type 2 diabetic patients. Modified Atkins diet showed superior benefit as regards improvement of HbA1c, HDL and CRP in comparison to the other dietary plans. [ABSTRACT FROM AUTHOR]

Isthmin‐1 (Ism1) plays roles in glucose uptake in mammals as an adipokine. To investigate its role in the glucose metabolism of common carp (Cyprinus carpio. L), the Ism1 sequence was cloned, and its expression and distribution in tissues were detected. In addition, we prepared and purified the recombinant Ism1 protein using the E. coli expression system and assessed changes in the expression of key genes related to glucose metabolism through both in vivo injection experiments and primary hepatocyte experiments in vitro. The results revealed that the open reading frame of Ism1 was 1377 bp long, encoding 458 amino acids. Similarity analysis indicated that Ism1 exhibited a close evolutionary relationship with goldfish (Carassius auratus), sharing 98.35% amino acid similarity. Ism1 was expressed in all tissues of common carp, with the highest level observed in the heart, followed by the gill, head kidney, and hepatopancreas. Distinct patterns of Ism1 expression were identified during the oral glucose tolerance test and long‐term high‐carbohydrate and high‐fat diet feeding experiments. In vivo studies demonstrated that the serum glucose concentration was reduced on treatment with Ism1, accompanied by a significant upregulation of mRNA levels for gk, hk, and pfk genes in hepatopancreas; conversely pepck and g6pase mRNA levels were significantly downregulated in the hepatopancreas under these conditions as well. Furthermore, our primary hepatocyte experiment confirmed that Ism1 could inhibit pepck and g6pase mRNA expression, while promoting gk, hk, and pfk mRNA expression levels. In conclusion, Ism1, in common carp, could participate in the glucose metabolism, which provides essential information for future studies on the function of Ism1. [ABSTRACT FROM AUTHOR]

Aim: Acyl‐coenzyme A dehydrogenase family member 10 (ACAD10) is a mitochondrial protein purported to be involved in the fatty acid oxidation pathway. Metformin is the most prescribed therapy for type 2 diabetes; however, its precise mechanisms of action(s) are still being uncovered. Upregulation of ACAD10 is a requirement for metformin's ability to inhibit growth in cancer cells and extend lifespan in Caenorhabditis elegans. However, it is unknown whether ACAD10 plays a role in metformin's metabolic actions. Materials and Methods: We assessed the role for ACAD10 on whole‐body metabolism and metformin action by generating ACAD10KO mice on a C57BL/6J background via CRISPR‐Cas9 technology. In‐depth metabolic phenotyping was conducted in both sexes on a normal chow and high fat‐high sucrose diet. Results: Compared with wildtype mice, we detected no difference in body composition, energy expenditure or glucose tolerance in male or female ACAD10KO mice, on a chow diet or high‐fat, high‐sucrose diet (p ≥.05). Hepatic mitochondrial function and insulin signalling was not different between genotypes under basal or insulin‐stimulated conditions (p ≥.05). Glucose excursions following acute administration of metformin before a glucose tolerance test were not different between genotypes nor was body composition or energy expenditure altered after 4 weeks of daily metformin treatment (p ≥.05). Despite the lack of a metabolic phenotype, liver lipidomic analysis suggests ACAD10 depletion influences the abundance of specific ceramide species containing very long chain fatty acids, while metformin treatment altered clusters of cholesterol ester, plasmalogen, phosphatidylcholine and ceramide species. Conclusions: Loss of ACAD10 does not alter whole‐body metabolism or impact the acute or chronic metabolic actions of metformin in this model. [ABSTRACT FROM AUTHOR]

The article discusses the importance of maintaining brain health for successful aging and business performance. It highlights the shift in focus from disease and decline to health and growth in research and policy efforts related to aging. The article emphasizes the impact of brain health on daily activities, independence, and physical health. It also explores various lifestyle factors that can promote brain health, such as physical activity, a healthy diet, not smoking, social engagement, and having a sense of purpose. The role of workplaces in promoting brain health is also discussed, with an emphasis on workplace design and its impact on brain health. The article concludes by mentioning the development of an Organizational Brain Health Best Practice Score to help organizations assess and improve their workforce brain health initiatives. [Extracted from the article]

Several studies have demonstrated the protective effects of melatonin against metabolic diseases, such as liver steatosis. However, its therapeutic effects have received less scrutiny. The present study aimed to explore melatonin's therapeutic effectiveness in treating non-alcoholic fatty liver disease (NAFLD) induced by a high-carbohydrate high-fat (HCHF) diet in rats. The NAFLD was developed in male Wistar rats using an HCHF diet for 8 weeks. Afterward, they were given melatonin orally for four weeks at doses of 5 mg/kg, 10 mg/kg, and 30 mg/kg, along with the HCHF diet. In addition, six age-matched healthy rats received the highest dose of melatonin (30 mg/kg) for the same duration. Rats on the HCHF diet exhibited obesity, dyslipidemia, hyperglycemia, glucose intolerance, insulin resistance, inflammation, oxidative stress, and liver injury (steatosis). Melatonin treatment at 10 mg/kg and 30 mg/kg reduced body weight, adiposity index, oxidative damage, and inflammation but did not affect impaired glucose metabolism induced by the HCHF diet. Meanwhile, the highest dose of melatonin (30 mg/kg) reduced the liver steatosis index in HCHF rats but caused mild liver damage in healthy rats. In conclusion, using melatonin demonstrated positive outcomes in treating NAFLD induced by the HCHF diet in rats, with no noteworthy effects observed in healthy rats. A moderate dosage of 10 mg/kg of melatonin proved to be a safer and more efficient method for reducing HCHF diet-induced NAFLD in rats. Higher melatonin doses should be cautiously administered due to potential disruptions in lipid metabolism and the risk of liver complications. [ABSTRACT FROM AUTHOR]

Obesity is defined as the abnormal and excessive accumulation of fat. Enlargement of white adipose tissue due to obesity activates the sympathetic nervous system to stimulate lipolysis to break down fat extensively. This causes a lot of free fatty acids to circulate in the body. Excessive circulating free fatty acids affect many cells and produce oxidative stress, which spreads throughout the body. This research purpose is to determine the anti-obesity and antioxidant activities of ethanol extract of B. pandurata rhizome (EEBP).

Background: Dietary imbalance, such as a lower proportion of complex carbohydrates and a higher protein diet, may contribute to gestational diabetes mellitus (GDM) risks through their metabolisms. However, there is a lack of knowledge regarding the association between butyrate, iso-butyrate, and GDM, which are metabolisms of the two primary nutrients above. This study aimed to clarify the association of butyrate and iso-butyrate with GDM. Methods: A nested case–control study was conducted based on the Beijing Birth Cohort Study (BBCS) from 2017 to 2018. Totally, 99 singleton women were involved (GDM: n = 49, control: n = 50). All participants provided blood samples twice (in their first and second trimesters). Gas chromatography-mass spectrometry (GC-MS) was used for butyrate and iso-butyrate detection. Unconditional logistic regression and receiver operating characteristic (ROC) curve analysis were used for statistical analysis. Results: The results showed that butyrate in the first trimester was negatively correlated with GDM (odds ratio (OR): 0.00, 95% confidential interval (CI): 0.00–0.21, P = 0.008), and iso-butyrate in the second trimester was positively related to GDM (OR: 627.68, 95% CI: 40.51–9724.56, P < 0.001). The ratio (butyrate/iso-butyrate) was negatively associated with GDM, both in the first trimester (OR: 0.00, 95%CI: 0.00–0.05, P < 0.001) and in the second trimester (OR: 0.52, 95% CI: 0.34–0.80, P = 0.003). The area under the curve (AUC) using the ratio in the first trimester combined with clinical risk factors achieved 0.89 (95% CI: 0.83–0.95). Iso-butyrate in the second trimester combined with clinical risk factors achieved an AUC of 0.97 (95% CI: 0.92–1.00). Conclusions: High iso-butyrate and low butyrate levels may be associated with an increased risk of GDM. As they are produced through dietary nutrient formation by gut microbiota, further studies on the association of dietary intake and butyrate or iso-butyrate concentration in plasma may help find a novel approach to nutritional intervention for GDM. [ABSTRACT FROM AUTHOR]

Depressive symptoms are a serious public mental health problem, and dietary intake is often considered to be associated with depressive symptoms. However, the relationship between the quality of dietary carbohydrates and depressive symptoms remains unclear. Therefore, this study aimed to investigate the relationship between high and low-quality carbohydrates and depressive symptoms and to attempt to construct an integrated model using machine learning to predict depressive symptoms. A total of 4982 samples from the National Health and Nutrition Examination Survey (NHANES) were included in this study. Carbohydrate intake was assessed by a 24-h dietary review, and depressive symptoms were assessed using the Patient Health Questionnaire-9 (PHQ9). Variance inflation factor (VIF) and Relief-F algorithms were used for variable feature selection. The results of multivariate linear regression showed a negative association between high-quality carbohydrates and depressive symptoms (β: −0.147, 95 % CI: −0.239, −0.056, p = 0.002) and a positive association between low-quality carbohydrates and depressive symptoms (β: 0.018, 95 % CI: 0.007, 0.280, p = 0.001). Subsequently, we used the XGboost model to produce a comprehensive depressive symptom evaluation model and developed a corresponding online tool (http://8.130.128.194:5000/) to evaluate depressive symptoms clinically. The cross-sectional study could not yield any conclusions regarding causality, and the model has not been validated with external data. Carbohydrate quality is associated with depressive symptoms, and machine learning models that combine diet with socioeconomic factors can be a tool for predicting depression severity. • Exploring the association between high and low carbohydrate diet quality and depressive symptom severity • Building an integrated economic society-diet machine learning model for predicting depression severity • Development of a convenient web-based model for predicting depression severity [ABSTRACT FROM AUTHOR]

Simple Summary: An excessive carbohydrate content in diets can have a negative effect on fish growth. In this study, the effects of berberine supplementation in high-carbohydrate diets on the growth performance, glucose metabolism, bile acid synthesis, liver transcriptome, and intestinal flora of Nile tilapia were investigated. Conclusion: An appropriate amount of berberine can stimulate the synthesis of bile acids by changing the structure of the intestinal flora of tilapia, thus promoting glycolysis and inhibiting gluconeogenesis, then regulating the blood glucose, which is beneficial to the growth of tilapia. This provides the data to improve carbohydrate utilization in tilapia and support the development of high-carbohydrate diets in aquaculture. Berberine is an alkaloid used to treat diabetes. This experiment aimed to investigate the effects of berberine supplementation in high-carbohydrate diets on the growth performance, glucose metabolism, bile acid synthesis, liver transcriptome, and intestinal flora of Nile tilapia. The six dietary groups were the C group with 29% carbohydrate, the H group with 44% carbohydrate, and the HB1-HB4 groups supplemented with 25, 50, 75, and 100 mg/kg of berberine in group H. The results of the 8-week trial showed that compared to group C, the abundance of Bacteroidetes was increased in group HB2 (p < 0.05). The cholesterol-7α-hydroxylase (CYP7A1) and sterol-27-hydroxylase (CYP27A1) activities were decreased and the expression of FXR was increased in group HB4 (p < 0.05). The pyruvate carboxylase (PC) and phosphoenolpyruvate carboxykinase (PEPCK) activities was decreased in group HB4 (p < 0.05). The liver transcriptome suggests that berberine affects carbohydrate metabolic pathways and primary bile acid synthesis pathways. In summary, berberine affects the glucose metabolism in tilapia by altering the intestinal flora structure, enriching differentially expressed genes (DEGs) in the bile acid pathway to stimulate bile acid production so that it promotes glycolysis and inhibits gluconeogenesis. Therefore, 100 mg/kg of berberine supplementation in high-carbohydrate diets is beneficial to tilapia. [ABSTRACT FROM AUTHOR]

Prediabetes is characterized by abnormal glycemic levels below the type 2 diabetes threshold, and effective control of blood glucose may prevent the progression to type 2 diabetes. While the association between the gut microbiota, glucose metabolism, and insulin resistance in diabetic patients has been established in previous studies, there is a lack of research regarding these aspects in prediabetic patients in Asia. We aim to investigate the composition of the gut microbiota in prediabetic patients and their differences compared to healthy individuals. In total, 57 prediabetic patients and 60 healthy adult individuals aged 18 to 65 years old were included in this study. Biochemistry data, fecal samples, and 3 days of food records were collected. Deoxyribonucleic acid extraction and next-generation sequencing via 16S ribosomal ribonucleic acid metagenomic sequencing were conducted to analyze the relationship between the gut microbiota and dietary habits. Prediabetic patients showed a lower microbial diversity than healthy individuals, with 9 bacterial genera being less abundant and 14 others more abundant. Prediabetic patients who consumed a low-carbohydrate (LC) diet exhibited higher diversity in the gut microbiota than those who consumed a high-carbohydrate diet. A higher abundance of Coprococcus was observed in the prediabetic patients on an LC diet. Compared to healthy individuals, the gut microbiota of prediabetic patients was significantly different, and adopting an LC diet with high dietary fiber consumption may positively impact the gut microbiota. Future studies should aim to understand the relationship between the gut microbiota and glycemic control in the Asian population. [ABSTRACT FROM AUTHOR]

Lipid and sugar homeostasis is critical for insect development and survival. In this study, we characterized an acetyl coenzyme A carboxylase gene in Blattella germanica (BgACC) that is involved in both lipogenesis and sugar homeostasis. We found that BgACC was dominantly expressed in the fat body and integument, and was significantly upregulated after molting. Knockdown of BgACC in 5th‐instar nymphs did not affect their normal molting to the next nymphal stage, but it caused a lethal phenotype during adult emergence. BgACC‐RNA interference (RNAi) significantly downregulated total free fatty acid (FFA) and triacylglycerol (TAG) levels, and also caused a significant decrease of cuticular hydrocarbons (CHCs). Repression of BgACC in adult females affected the development of oocytes and resulted in sterile females, but BgACC‐RNAi did not affect the reproductive ability of males. Interestingly, knockdown of BgACC also changed the expression of insulin‐like peptide genes (BgILPs), which mimicked a physiological state of high sugar uptake. In addition, BgACC was upregulated when B. germanica were fed on a high sucrose diet, and repression of BgACC upregulated the expression of the glycogen synthase gene (BgGlyS). Moreover, BgACC‐RNAi increased the circulating sugar levels and glycogen storage, and a longevity assay suggested that BgACC was important for the survival of B. germanica under conditions of high sucrose uptake. Our results confirm that BgACC is involved in multiple lipid biogenesis and sugar homeostasis processes, which further modulates insect reproduction and sugar tolerance. This study benefits our understanding of the crosstalk between lipid and sugar metabolism. [ABSTRACT FROM AUTHOR]

Background: Adequate level of carbohydrates in aquafeeds help to conserve protein and reduce cost. However, studies have indicated that high-carbohydrate (HC) diet disrupt the homeostasis of the gut–liver axis in largemouth bass, resulting in decreased intestinal acetate and butyrate level. Method: Herein, we had concepted a set of feeding experiment to assess the effects of dietary sodium acetate (SA) and sodium butyrate (SB) on liver health and the intestinal microbiota in largemouth bass fed an HC diet. The experimental design comprised 5 isonitrogenous and isolipidic diets, including LC (9% starch), HC (18% starch), HCSA (18% starch; 2 g/kg SA), HCSB (18% starch; 2 g/kg SB), and HCSASB (18% starch; 1 g/kg SA + 1 g/kg SB). Juvenile largemouth bass with an initial body weight of 7.00 ± 0.20 g were fed on these diets for 56 d. Results: We found that dietary SA and SB reduced hepatic triglyceride accumulation by activating autophagy (ATG101, LC3B and TFEB), promoting lipolysis (CPT1α, HSL and AMPKα), and inhibiting adipogenesis (FAS, ACCA, SCD1 and PPARγ). In addition, SA and SB decreased oxidative stress in the liver (CAT, GPX1α and SOD1) by activating the Keap1-Nrf2 pathway. Meanwhile, SA and SB alleviated HC-induced inflammation by downregulating the expression of pro-inflammatory factors (IL-1β, COX2 and Hepcidin1) through the NF-κB pathway. Importantly, SA and SB increased the abundance of bacteria that produced acetic acid and butyrate (Clostridium_sensu_stricto_1). Combined with the KEGG analysis, the results showed that SA and SB enriched carbohydrate metabolism and amino acid metabolism pathways, thereby improving the utilization of carbohydrates. Pearson correlation analysis indicated that growth performance was closely related to hepatic lipid deposition, autophagy, antioxidant capacity, inflammation, and intestinal microbial composition. Conclusions: In conclusion, dietary SA and SB can reduce hepatic lipid deposition; and alleviate oxidative stress and inflammation in largemouth bass fed on HC diet. These beneficial effects may be due to the altered composition of the gut microbiota caused by SA and SB. The improvement effects of SB were stronger than those associated with SA. [ABSTRACT FROM AUTHOR]

We studied the effect of separate and combined influence of chronic forced physical activity reduction and high-fat and high-carbohydrate diet containing cholesterol on some indicators of carbohydrate, lipid, and cholesterol metabolism in growing male Wistar rats. Used combination of factors simulating a sedentary lifestyle and unhealthy diet did not have a synergistic effect on the selected biomarkers. On the contrary, the effect was antagonistic: body weight and appetite decreased and insulin resistance increased. The obtained results indicate certain prospects of hypercholesterolemia model using in preclinical studies of specialized food products to optimize the diet of individuals with disorders of carbohydrate and lipid metabolism. [ABSTRACT FROM AUTHOR]

Older women and Black individuals are more likely to experience frailty. A metabolomic characterization of frailty may help inform more effective interventions aimed at improving health, reducing disparities, and preventing frailty with aging. We sought to identify metabolites and pathways associated with vigor to frailty and determine whether associations differed by sex and/or race among n = 2189 older Black and White men and women from the Health, Aging, and Body Composition (Health ABC) study. Fasting plasma metabolites were measured using liquid chromatography-mass spectrometry. Vigor to frailty was based on weight change, physical activity, gait speed, grip strength, and usual energy. We used linear regression of a single metabolite on vigor to frailty, adjusting for age, sex, race, study site, and multiple comparisons using a Bonferroni correction. Among 500 metabolites, 113 were associated with vigor to frailty (p < 0.0001). Associations between metabolites and vigor to frailty did not differ significantly by race and/or sex. Lower amino acids, glycerophospholipids, sphingolipids, and dehydroepiandrosterone sulfate and higher acylcarnitines, fatty acids, amino acid derivatives, organic acids, carbohydrates, citric acid cycle metabolites, and trimethylamine oxide were associated with frailer scores. Pathway analyses identified the citric acid cycle as containing more frailty-associated metabolites than expected by chance (p = 0.00005). Calories and protein intake did not differ by vigor to frailty. Frailer Health ABC participants may have lower utilization of energy pathways, potentially as a result of less demand and less efficient utilization of similar amounts of nutrients when compared to more vigorous participants. [ABSTRACT FROM AUTHOR]

Cellular senescence and iron accumulation were separately observed in diabetic nephropathy (DN). Limited evidence supports that iron was significantly accumulated in senescent cells. We aimed to explore whether iron is involved in the pathogenesis role of senescence in DN. Renal cells were treated with high glucose (HG, 35 mM) for 10 or 15 days, and DN mice were induced by high-fat diet and streptozotocin. Gene ontology enrichment, gene set enrichment analysis analysis, β-galactosidase staining, 5-ethynyl-2-deoxyuridine staining, and western blot depicted the upregulated senescence pathway in vitro and in vivo of DN. Lactate dehydrogenase (LDH) release was increased by HG and reversed by p16/p21 knockdown, and the supernatant of HG-treated cells caused increased LDH release from normal cells. Iron metabolism-related protein expression was disordered after HG exposure concomitant with senescence. Ferric ammonium citrate (50 μM) upregulated gamma-H2A.X variant histone and increased the senescence markers in HG-treated cells. The treatment of deferoxamine (0.5 μM) had the opposite effect. Compared to the non-DN individual, increased ferritin and senescence markers were verified in DN mice and patients, and the co-localization of ferritin and senescence markers was observed by immunofluorescence. These results suggested that accumulated iron was correlated with aggravated DNA damage and accelerated senescence, and revealed the role of iron in the cellular senescence of diseases. [ABSTRACT FROM AUTHOR]