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Polygonatum sibiricum, a plant homologous to both medicine and food, is of significant importance. Its primary active components include polysaccharides, saponin, flavonoids, polyphenols, and alkaloids. These constituents are known for their roles in enhancing immune function, combating fatigue, providing anti-oxidative benefits, reducing blood sugar, and offering anti-inflammatory effects. Consequently, P. sibiricum presents wide-ranging prospects in health food and pharmaceutical research and development. This paper provides a comprehensive summary of research advancements in the polysaccharides, flavonoids, saponins, and solomonseal rhizome extract of P. sibiricum, particularly in metabolic regulation. It delves into the mechanisms by which the main active substances of P. sibiricum influence glucose and lipid metabolism. Simultaneously, the paper analyzes current patents and the state of industrial development related to P. sibiricum, aiming to provide a reference for future research and development of metabolic regulation functional products based on this plant. [ABSTRACT FROM AUTHOR]

Globally, type 2 diabetes mellitus (T2DM) is a major threat to the public's health, particularly in low- and middle-income countries (LMICs). The production of short-chain fatty acids (SCFAs) by the gut microbiota has been reported to have the potential to reduce the prevalence of T2DM, particularly in LMICs where the disease is becoming more common. Dietary fibers are the primary source of SCFAs; they can be categorized as soluble (such as pectin and inulin) or insoluble (such as resistant starches). Increased consumption of processed carbohydrates, in conjunction with insufficient consumption of dietary fiber, has been identified as a significant risk factor for type 2 diabetes (T2DM). However, there are still controversies over the therapeutic advantages of SCFAs on human glucose homeostasis, due to a lack of studies in this area. Hence, a few questions need to be addressed to gain a better understanding of the beneficial link between SCFAs and glucose metabolism. These include the following: What are the biochemistry and biosynthesis of SCFAs? What role do SCFAs play in the pathology of T2DM? What is the most cost-effective strategy that can be employed by LMICs with limited laboratory resources to enhance their understanding of the beneficial function of SCFAs in patients with T2DM? To address the aforementioned questions, this paper aims to review the existing literature on the protective roles that SCFAs have in patients with T2DM. This paper further discusses possible cost-effective and accurate strategies to quantify SCFAs, which may be recommended for implementation by LMICs as preventive measures to lower the risk of T2DM. [ABSTRACT FROM AUTHOR]

Simple Summary: Obesity is a global concern within human, pet, and horse populations. A major consequence of obesity is a disruption to glucose and insulin metabolisms, leading to metabolic conditions including insulin resistance and/or diabetes. This paper discusses these consequences of obesity and excess adipose tissue both in idle and athletic subjects. Exercise conditioning can improve glucose metabolism and insulin sensitivity. Regular exercise can also facilitate weight loss, wherein the reduction of adipose tissue alleviates fat's negative impacts on metabolism, while also decreasing the mechanical load on a subject's limbs. These actions could result in better health, reduced incidence of metabolic disease, and, perhaps, improved performance. Obesity is an important health concern in horses, along with humans and companion animals. Adipose tissue is an inflammatory organ that alters the insulin-signaling cascade, ultimately causing insulin dysregulation and impaired glucose metabolism. These disruptions can increase the risk of metabolic disease and laminitis in horses and may also impact energy metabolism during exercise. A single bout of exercise, along with chronic exercise conditioning, increases insulin sensitivity and glucose disposal via both contraction- and insulin-mediated glucose uptake pathways. Regular exercise also increases calorie expenditure, which can facilitate weight (as body fat) loss. This paper explores the metabolic pathways affected by adiposity, as well as discusses the impact of exercise on insulin metabolism in horses. [ABSTRACT FROM AUTHOR]

An increasing number of studies have reported that androgens and androgen receptors (AR) play important roles in the regulation of glucose and lipid metabolism. Impaired glucose and lipid metabolism and the development of obesity-related diseases have been found in either hypogonadal men or male rodents with androgen deficiency. Exogenous androgens supplementation can effectively improve these disorders, but the mechanism by which androgens regulate glucose and lipid metabolism has not been fully elucidated. Mitochondria, as powerhouses within cells, are key organelles influencing glucose and lipid metabolism. Evidence from both pre-clinical and clinical studies has reported that the regulation of glucose and lipid metabolism by androgens/AR is strongly associated with the impact on the content and function of mitochondria, but few studies have systematically reported the regulatory effect and the molecular mechanism. In this paper, we review the effect of androgens/AR on mitochondrial content, morphology, quality control system, and function, with emphases on molecular mechanisms. Additionally, we discuss the sex-dimorphic effect of androgens on mitochondria. This paper provides a theoretical basis for shedding light on the influence and mechanism of androgens on glucose and lipid metabolism and highlights the mitochondria-based explanation for the sex-dimorphic effect of androgens on glucose and lipid metabolism. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The increasing prevalence of bariatric surgery among women of childbearing age raises critical questions about the correct management of pregnancy following these procedures. This literature review delves into the multifaceted considerations surrounding pregnancy after bariatric surgery, with a particular focus on the importance of preconception counselling, appropriate nutrition assessment, and the necessity of correct folic acid supplementation. Key areas of investigation include nutrient absorption challenges, weight gain during pregnancy, and potential micronutrient deficiencies. Examining the relationship between bariatric surgery and birth defects, particularly heart and musculoskeletal issues, uncovers a twofold increase in risk for women who underwent surgery before pregnancy, with the risk emphasized before folic acid fortification. In contrast, a nationwide study suggests that infants born to mothers with bariatric surgery exhibit a reduced risk of major birth defects, potentially associated with improved glucose metabolism. In addition, this review outlines strategies for managing gestational diabetes and other pregnancy-related complications in individuals with a history of bariatric surgery. By synthesizing existing literature, this paper aims to provide healthcare providers with a comprehensive framework for the correct management of pregnancy in this unique patient population, promoting the health and well-being of both mother and child. [ABSTRACT FROM AUTHOR]

Known as a classic product of glucose metabolism, lactic acid has been regarded as a metabolic waste. However, it wasn't until the discovery of Warburg effect in tumors that researchers refocused on the role of lactic acid in cells. Being a kind of signaling molecule with multiple functions, lactic acid is a key metabolic product connecting glycolysis and oxidative phosphorylation, and it also has non-metabolic activity. Recent studies have shown that lactic acid can be used as a substrate to participate in a novel post-translational modification of proteins, known as protein lactylation. It can be involved in many kinds of diseases, and plays an important role in immune regulation and homeostasis maintenance. This paper briefly describes and summarizes the important role of lactylation modification in the developmental mechanisms of diseases such as tumors, inflammation, neuropsychiatric diseases, cardiocerebrovascular diseases, and so on. [ABSTRACT FROM AUTHOR]

Otto Warburg published the first paper describing what became known as the Warburg effect in 1923. All that was known about glucose metabolism at that time was that it occurred in two stages: (i) fermentation (glycolysis) in which glucose was converted to lactate, which did not require oxygen, and (ii) oxidative metabolism, in which the carbon atoms derived from glycolysis were fully oxidized to carbon dioxide, which did require oxygen. Warburg discovered that most tumour tissues produced a large amount of lactate that was reduced but not eliminated in the presence of oxygen, while most normal tissues produced a much smaller amount of lactate that was eliminated by the provision of oxygen. These findings were clearly well ahead of their time because it was another 80 years before they were to have any major impact, and even today the mechanisms underlying the Warburg effect are not completely understood. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is a complex autoimmune disease that presents significant challenges for both patients and health care providers. The absence of functional β-cells in the pancreas results in a lifelong struggle for glucose regulation and necessitates meticulous management for survival. This paper highlights the intricacies of glucose regulation and the difficulties in maintaining stable blood glucose levels through exogenous means. Moreover, it explores the limitations faced by health care providers in managing T1D, leading to a superficial approach to care. The ultimate cure for T1D lies in prevention, although our current understanding of its etiology remains incomplete. By adopting an integrative approach to T1D care, health care providers can play a vital role in enhancing the management of this chronic condition. This paper aims to inspire a holistic perspective on T1D care and encourage further exploration and implementation of integrative strategies to improve the lives of individuals living with this complex disease. [ABSTRACT FROM AUTHOR]

Copyright of Feed Research is the property of Editorial Board of Feed Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Glucose is the most important biological energy donor, is the source of energy and metabolism of living cells, and plays an important role in cell signaling. Abnormal glucose metabolism is frequently associated with diabetes mellitus, retinopathy, Alzheimer's disease, and cardiovascular diseases. Sodium-glucose cotransporter 2 (SGLT2) is one of the transporters involved in the maintenance of glucose homeostasis. It mediates the reabsorption of glucose by the kidney and plays an important role in maintaining the stability of plasma glucose. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) can reduce the reabsorption of glucose in the kidney and have a positive impact on blood glucose, blood pressure, body weight, etc. This paper summarizes the current research progress of SGLT2 and its inhibitors, the structure and key sites of SGLT2 and the mechanism of SGLT2i. In particular, in recent years, it is found that the protective effect of SGLT2i on kidney and cardiovascular is more obvious, and it can also resist the occurrence and development of tumor cells. Finally, this paper summarises and discusses the current bottlenecks in research related to SGLT2i and provides new ideas for future structure-based drug optimisation of inhibitors. [ABSTRACT FROM AUTHOR]

Diabetes Mellitus (DM) is amongst the most notable causes of years of life lost worldwide and its prevalence increases perpetually. The disease is characterized as multisystemic dysfunctions attributed to hyperglycemia resulting directly from insulin resistance (IR), inadequate insulin secretion, or enormous glucagon secretion. Insulin is a highly anabolic peptide hormone that regulates blood glucose levels by hastening cellular glucose uptake as well as controlling carbohydrate, protein, and lipid metabolism. In the course of Type 2 Diabetes Mellitus (T2DM), which accounts for nearly 90% of all cases of diabetes, the insulin response is inadequate, and this condition is defined as Insulin Resistance. IR sequela include, but are not limited to, hyperglycemia, cardiovascular system impairment, chronic inflammation, disbalance in oxidative stress status, and metabolic syndrome occurrence. Despite the substantial progress in understanding the molecular and metabolic pathways accounting for injurious effects of IR towards multiple body organs, IR still is recognized as a ferocious enigma. The number of widely available therapeutic approaches is growing, however, the demand for precise, safe, and effective therapy is also increasing. A literature search was carried out using the MEDLINE/PubMed, Google Scholar, SCOPUS and Clinical Trials Registry databases with a combination of keywords and MeSH terms, and papers published from February 2021 to March 2022 were selected as recently published papers. This review paper aims to provide critical, concise, but comprehensive insights into the advances in the treatment of IR that were achieved in the last months. [ABSTRACT FROM AUTHOR]

Mannose, a different isomer of the hydroxyl group at the C-2 position of glucose, shares the same transport carrier protein with glucose to enter cells and participate in the regulation of glucose metabolism. It affects cell growth, differentiation, and function and plays an active role in tumor immunity and inflammatory processes. This paper provides theoretical support for expanding the clinical applications of mannose by exploring its constitution, metabolic pathways, and role in regulating immune cell function and treating immunology-related diseases. [ABSTRACT FROM AUTHOR]

Dendrobium officinale is a perennial epiphytic herb of Dendrobium genus of Orchidaceae, which enjoys the reputation of life-saving herb' in China's folklore. It contains polysaccharides, alkaloids, flavonoids and other bioactive ingredients, which together make it good at improving immunity, balancing inflammation, regulating glucose and lipid metabolism, and promoting the health of gastrointestinal tract, ect. On November 9 2023, Dendrobium was officially added as 'food and medicine of the same origin' substance, which expanded its application prospects in the field of healthy food by the National Health and Health Commission of the People's Republic of China and State Administration for Market Regulation. This paper summarized the research history of Dendrobium officinale from 'cultivation and planting' to 'its functional components' and 'its processing characteristics', and also summarized the research progress of its main functional substance, Dendrobium officinale polysaccharide, in all aspects. At the same time, this paper also elaborated the current situation of Dendrobium herb deep-processing, and analyzed the key problem and future direction of Dendro¬bium officinale industrialization, in order to provide reference for the innovative application of Dendrobium officinale in the health industry. [ABSTRACT FROM AUTHOR]

Laboratory animal research with nonhuman primates (NHPs) requires anesthesia for most procedures to ensure safety and consistency in sample collection. However, anesthesia drugs can have adverse effects on the physiological measures of interest. Alfaxalone, most notably used in dogs and cats, offers rapid onset, short duration of action, and has a high safety margin. Here, we compared our current anesthesia protocol using Telazol, to three different doses of alfaxalone during a one-hour intravenous glucose tolerance test, the standard evaluation of glucose metabolism in NHPs. Results indicate there are no differences in the rate of glucose metabolism, anesthesia depth measurements, or total duration of sedation, but induction, number of supplemental doses required, and recovery time to eating were affected by the different doses of alfaxalone. Cardiovascular measures showed variability between the four protocols in respiratory rate and systolic blood pressure rates only. These results indicate that alfaxalone can produce a reliable state of anesthesia, similar to our current protocol, and confers minimal cardiovascular or metabolic disturbance, as well as enhanced recovery characteristics. As such, alfaxalone is a promising anesthetic for use in laboratory animals and further investigation is warranted. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is a progressive metabolic disease characterized by hepatic steatosis, inflammation, and fibrosis that seriously endangers global public health. Epidemiological studies have shown that the incidence of non-alcoholic fatty liver disease in postmenopausal women has significantly increased. Studies have shown that estrogen deficiency is the main reason for this situation, and supplementing estrogen has become a new direction for preventing the occurrence of postmenopausal fatty liver. However, although classical estrogen replacement therapy can reduce the incidence of postmenopausal NAFLD, it has the risk of increasing stroke and cardiovascular diseases, so it is not suitable for the treatment of postmenopausal NAFLD. More and more recent studies have provided evidence that phytoestrogens are a promising method for the treatment of postmenopausal NAFLD. However, the mechanism of phytoestrogens in preventing and treating postmenopausal NAFLD is still unclear. This paper summarizes the clinical and basic research evidence of phytoestrogens and reviews the potential therapeutic effects of phytoestrogens in postmenopausal NAFLD from six angles: enhancing lipid metabolism in liver and adipose tissue, enhancing glucose metabolism, reducing oxidative stress, reducing the inflammatory response, regulating intestinal flora, and blocking liver fibrosis (Graphical Abstract). [ABSTRACT FROM AUTHOR]

In this paper, we investigate the disruption of the glucose homeostasis at the whole-body level by the presence of cancer disease. Of particular interest are the potentially different responses of patients with or without hyperglycemia (including diabetes mellitus) to the cancer challenge, and how tumor growth, in turn, responds to hyperglycemia and its medical management. We propose a mathematical model that describes the competition between cancer cells and glucose-dependent healthy cells for a shared glucose resource. We also include the metabolic reprogramming of healthy cells by cancer-cell-initiated mechanism to reflect the interplay between the two cell populations. We parametrize this model and carry out numerical simulations of various scenarios, with growth of tumor mass and loss of healthy body mass as endpoints. We report sets of cancer characteristics that show plausible disease histories. We investigate parameters that change cancer cells’ aggressiveness, and we exhibit differing responses in diabetic and non-diabetic, in the absence or presence of glycemic control. Our model predictions are in line with observations of weight loss in cancer patients and the increased growth (or earlier onset) of tumor in diabetic individuals. The model will also aid future studies on countermeasures such as the reduction of circulating glucose in cancer patients. [ABSTRACT FROM AUTHOR]

Epilepsy is a common and severe neurological disorder in which impaired glucose metabolism leads to changes in neuronal excitability that slow or promote the development of epilepsy. Leptin and adiponectin are important mediators regulating glucose metabolism in the peripheral and central nervous systems. Many studies have reported a strong association between epilepsy and these two adipokines involved in multiple signaling cascades and glucose metabolism. Due to the complex regulatory mechanisms between them and various signal activation networks, their role in epilepsy involves many aspects, including the release of inflammatory mediators, oxidative damage, and neuronal apoptosis. This paper aims to summarize the signaling pathways involved in leptin and adiponectin and the regulation of glucose metabolism from the perspective of the pathogenesis of epilepsy. In particular, we discuss the dual effects of leptin in epilepsy and the relationship between antiepileptic drugs and changes in the levels of these two adipokines. Clinical practitioners may need to consider these factors in evaluating clinical drugs. Through this review, we can better understand the specific involvement of leptin and adiponectin in the pathogenesis of epilepsy, provide ideas for further exploration, and bring about practical significance for the treatment of epilepsy, especially for the development of personalized treatment according to individual metabolic characteristics. [ABSTRACT FROM AUTHOR]

Ferroptosis is a new type of iron-dependent cell death and is involved in many biological processes. Multiple ferroptosis signals affect enzymes and metabolites during glucose metabolism, altering the metabolic pathways of macrophages. In addition, macrophages with different polarization phenotypes have different resistance to ferroptosis, which affects the occurrence and signal transmission of ferroptosis. Therefore, the important process of glucose metabolism in macrophages is targeted to regulate the sensitivity of macrophages to ferroptosis through energy metabolism. In this paper, we review the recent research progress on the effect of ferroptosis signaling on the reprogramming of glucose metabo, lism in macrophages and the regulatory effects of various compounds. [ABSTRACT FROM AUTHOR]

Ensuring a robust and reliable evaluation of coma deepness and prognostication of neurological outcome is challenging. We propose to develop PET neuroimaging as a new diagnostic and prognosis tool for comatose patients using a recently published methodology to perform functional PET (fPET). This exam permits the quantification of task-specific changes in neuronal metabolism in a single session. The aim of this protocol is to determine whether task-specific changes in glucose metabolism during the acute phase of coma are able to predict recovery at 18 months. Participation will be proposed for all patients coming for a standard PET-CT in our center in order to evaluate global cerebral metabolism during the comatose state. Legally appointed representative consent will be obtained to slightly modify the exam protocol: (1) 18F-fluorodeoxyglucose (18F-FDG) bolus plus continuous infusion instead of a simple bolus and (2) more time under camera to perform dynamic acquisition. Participants will undergo a 55-min fPET session with a 20% bolus + 80% infusion protocol. Two occurrences of three block (5-min rest, 10-min auditory stimulation and 10-min emotional auditory stimulation) will be performed after reaching equilibrium of FDG arterial concentration. We will compare the regional brain metabolism at rest and during the sessions of auditory and emotional auditory stimulation to search for a determinant of coma recovery (18 months of follow-up after the exam). Emotional auditory stimulation should induce an activation of: the auditory cortex, the consciousness areas and the neural circuitry for emotion (function to coma deepness). An activation analysis will be carried out to highlight regional brain activation using dedicated custom-made software based on Python statistical and image processing toolboxes. The association between activation levels and the Coma Recovery Scale-Revisited (CRS-R) will be assessed using multivariate analysis. If successful, the results from this study will help improve coma prognosis evaluation based on the pattern of neuronal metabolism at the onset of the pathology. The study protocol, rationale and methods are described in this paper. [ABSTRACT FROM AUTHOR]

Purpose: To give a comprehensive literature overview of alterations in regional cerebral glucose metabolism, measured using [18F]FDG PET, in conditions associated with hyperkinetic movement disorders and ataxia. In addition, correlations between glucose metabolism and clinical variables as well as the effect of treatment on glucose metabolism are discussed. Methods: A systematic literature search was performed according to PRISMA guidelines. Studies concerning tremors, tics, dystonia, ataxia, chorea, myoclonus, functional movement disorders, or mixed movement disorders due to autoimmune or metabolic aetiologies were eligible for inclusion. A PubMed search was performed up to November 2021. Results: Of 1240 studies retrieved in the original search, 104 articles were included. Most articles concerned patients with chorea (n = 27), followed by ataxia (n = 25), dystonia (n = 20), tremor (n = 8), metabolic disease (n = 7), myoclonus (n = 6), tics (n = 6), and autoimmune disorders (n = 5). No papers on functional movement disorders were included. Altered glucose metabolism was detected in various brain regions in all movement disorders, with dystonia-related hypermetabolism of the lentiform nuclei and both hyper- and hypometabolism of the cerebellum; pronounced cerebellar hypometabolism in ataxia; and striatal hypometabolism in chorea (dominated by Huntington disease). Correlations between clinical characteristics and glucose metabolism were often described. [18F]FDG PET-showed normalization of metabolic alterations after treatment in tremors, ataxia, and chorea. Conclusion: In all conditions with hyperkinetic movement disorders, hypo- or hypermetabolism was found in multiple, partly overlapping brain regions, and clinical characteristics often correlated with glucose metabolism. For some movement disorders, [18F]FDG PET metabolic changes reflected the effect of treatment. [ABSTRACT FROM AUTHOR]

This paper proposes a fractional-order model of glucose–insulin interaction. In Caputo's meaning, the fractional derivative is defined. This model arises in Bergman's minimal model, used to describe blood glucose and insulin metabolism, after intravenous tolerance testing. We showed that the established model has existence, uniqueness, non-negativity, and boundedness of fractional-order model solutions. The model's local and global stability was investigated. The parametric conditions under which a Hopf bifurcation occurs in the positive steady state for a proposed model are studied. Moreover, we present a numerical treatment for solving the proposed fractional model using the generalized Euler method (GEM). The model's local stability and Hopf bifurcation of the proposed model in sense of the GEM are presented. Finally, numerical simulations of the model using the Adam–Bashforth–Moulton predictor corrector scheme and the GEM have been presented to support our analytical results. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The reduction of the cerebral glucose metabolism is closely related to the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in Alzheimer's disease (AD); however, its underlying mechanism remains unclear. In this paper, 18F-flurodeoxyglucose positron emission tomography was used to trace cerebral glucose metabolism in vivo, along with Western blotting and immunofluorescence assays to examine the expression and distribution of associated proteins. Glucose and insulin tolerance tests were carried out to detect insulin resistance, and the Morris water maze was used to test the spatial learning and memory ability of the mice. The results show increased NLRP3 inflammasome activation, elevated insulin resistance, and decreased glucose metabolism in 3×Tg-AD mice. Inhibiting NLRP3 inflammasome activation using CY-09, a specific inhibitor for NLRP3, may restore cerebral glucose metabolism by increasing the expression and distribution of glucose transporters and enzymes and attenuating insulin resistance in AD mice. Moreover, CY-09 helps to improve AD pathology and relieve cognitive impairment in these mice. Although CY-09 has no significant effect on ferroptosis, it can effectively reduce fatty acid synthesis and lipid peroxidation. These findings provide new evidence for NLRP3 inflammasome as a therapeutic target for AD, suggesting that CY-09 may be a potential drug for the treatment of this disease. [ABSTRACT FROM AUTHOR]

Autophagy is an evolutionarily conserved process that plays a role in regulating homeostasis under physiological conditions. However, dysregulation of autophagy is observed in the development of human diseases, especially cancer. Autophagy has reciprocal functions in cancer and may be responsible for either survival or death. Hepatocellular carcinoma (HCC) is one of the most lethal and common malignancies of the liver, and smoking, infection, and alcohol consumption can lead to its development. Genetic mutations and alterations in molecular processes can exacerbate the progression of HCC. The function of autophagy in HCC is controversial and may be both tumor suppressive and tumor promoting. Activation of autophagy may affect apoptosis in HCC and is a regulator of proliferation and glucose metabolism. Induction of autophagy may promote tumor metastasis via induction of EMT. In addition, autophagy is a regulator of stem cell formation in HCC, and pro-survival autophagy leads to cancer cell resistance to chemotherapy and radiotherapy. Targeting autophagy impairs growth and metastasis in HCC and improves tumor cell response to therapy. Of note, a large number of signaling pathways such as STAT3, Wnt, miRNAs, lncRNAs, and circRNAs regulate autophagy in HCC. Moreover, regulation of autophagy (induction or inhibition) by antitumor agents could be suggested for effective treatment of HCC. In this paper, we comprehensively review the role and mechanisms of autophagy in HCC and discuss the potential benefit of targeting this process in the treatment of the cancer. 7tteT1Ytct-EF9p2vYhF_D Video Abstract [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

While brain glucose metabolism is known to contribute the carbons to support brain saturated and monounsaturated fatty biosynthesis de novo in the developing brains of young rodents, such a contribution to fatty acid biosynthesis in the adult brain is poorly understood. Recent work from the Bazinet laboratory illuminates the role of brain glucose metabolism in providing a carbon source from which palmitic acid is synthesized. In "The Majority of Brain Palmitic Acid is Maintained by Lipogenesis from Dietary Sugars and is Augmented in Offspring fed low Palmitic Acid Levels from Birth", the Bazinet lab demonstrates the importance of glucose as a key contributing source of carbon for brain palmitic synthesis and that a low palmitate diet exacerbates its utilization for brain palmitate synthesis de novo. Further, this impact is found in male mice rather than female mice, which adds an additional layer of importance. Mammals are known to conserve carbon and the brain has the ability to convert a variety of carbon sources to needed molecules, depending on the physiological needs of the brain. Overall, this paper contributes an important missing piece of the puzzle regarding carbon recycling in the brain and is a key piece of evidence that indeed the adult mammalian brain can convert glucose to carbons for use in saturated fatty acid synthesis. [ABSTRACT FROM AUTHOR]

Amyloid-β (Aβ) and tau are important biomarkers to predict the progression of cognitively unimpaired (CU) to dementia due to Alzheimer's disease (AD), according to the diagnosis framework from the US National Institute on Aging and the Alzheimer's Association (NIA-AA). However, it is clinically difficult to predict those subjects who were already with Aβ positive (A +) or tau positive (T +). As a typical characteristic of neurodegeneration in the diagnosis framework, the hypometabolism of the posterior cingulate cortex (PCC) has significant clinical value in the early prediction and prevention of AD. In this paper, we proposed the glucose metabolism in the PCC as a biomarker supplement to Aβ and tau biomarkers. First, we calculated the standard uptake value ratio (SUVR) of PCC based on fluorodeoxyglucose positron emission computed tomography (FDG PET) imaging. Secondly, we performed Kaplan–Meier (KM) survival analyses to explore the predictive performance of PCC SUVR, and the hazard ratio (HR) was calculated. Finally, we performed Pearson correlation analyses to explore the physiological significance of PCC SUVR. As a result, the PCC SUVR showed a consistent downward trend along the AD continuum. KM analyses showed better predictive performance when we combined PCC SUVR with cerebro-spinal fluid (CSF) Aβ42 (from HR = 2.56 to 3.00 within 5 years; from HR = 2.76 to 4.20 within 10 years) and ptau-181 (from 2.83 to 3.91 within 5 years; from HR = 2.32 to 4.17 within 10 years). There was a slight correlation between Aβ42/Aβ40 and PCC SUVR (r = 0.14, p = 0.02). In addition, several cognition scales were also correlated to PCC SUVR (from r = –0.407 to 0.383, p < 0.05). Our results showed that glucose metabolism in PCC may be a potential biomarker supplement to the Aβ and tau biomarkers to predict the progression of CU to AD. [ABSTRACT FROM AUTHOR]

Exosomes are a class of extracellular vesicles with a diameter of 50–100 nm secreted by various cells. They are generated through complex intracellular production mechanisms before being secreted to the extracellular environment. Due to their inclusion of proteins, lipids, and nucleic acids, exosomes play an important role in intercellular communication. Pancreatic β-cells play an irreplaceable role in the body's glucose metabolism. Their dysfunction is one of the causes of diabetes. Exosomes of various cells regulate the function of β-cells by regulating autoimmunity, delivering non-coding RNAs, or directly regulating intracellular signal pathways. This communication between β-cells and other cells plays an important role in the pathogenesis and development of diabetes, and has potential for clinical application. This paper reviews the biological sources and functions of exosomes, as well as intercellular crosstalk between β-cells and other cells that is involved in β-cell failure and regeneration. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Globally, the incidence of diabetes is increasing annually, and China has the largest number of patients with diabetes. Patients with type 2 diabetes need lifelong medication, with severe cases requiring surgery. Diabetes treatment may cause complications, side-effects, and postoperative sequelae that could lead to adverse health problems and significant social and economic burdens; thus, more efficient hypoglycemic drugs have become a research hotspot. Glucose metabolism disorders can promote diabetes, a systemic metabolic disease that impairs the function of other organs, including the heart, liver, and kidneys. Cyclocarya paliurus leaves have gathered increasing interest among researchers because of their effectiveness in ameliorating glucose metabolism disorders. At present, various compounds have been isolated from C. paliurus, and the main active components include polysaccharides, triterpenes, flavonoids, and phenolic acids. C. paliurus mainly ameliorates glucose metabolism disorders by reducing glucose uptake, regulating blood lipid levels, regulating the insulin signaling pathway, reducing β-cell apoptosis, increasing insulin synthesis and secretion, regulating abundances of intestinal microorganisms, and exhibiting α-glucosidase inhibitor activity. In this paper, the mechanism of glucose metabolism regulation by C. paliurus was reviewed to provide a reference to prevent and treat diabetes, hyperlipidaemia, obesity, and other metabolic diseases. [ABSTRACT FROM AUTHOR]

Copyright of Feed Research is the property of Editorial Board of Feed Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Natural drug research is one of the main directions for the discovery and development of new drugs. Underutilized vegetables with a rich source of medicinal value have drawn much attention from scientists in synthesizing new drugs and finding new pharmacological actions. Apigenin is a natural flavonoid with pharmacological effects including anti-inflammatory, anti-tumor, anti-oxidation, anti-radiation, antidepressant effect, cardiovascular protection, regulated glucose and lipid metabolism, protecting the kidneys, neuroprotection, antibacterial, etc. Thus, these pharmacological effects of apigenin and the interaction between apigenin and drugs were mainly reviewed in this paper. The pharmacological actions of apigenin are being elucidated not only on the molecular level but also on the apigenin-receptor interaction, changes in factors, enzymes, proteins, cells, or tissues. The apigenin derivatives and complexes with their pharmacological actions were also summarized, which is expected to provide a reference for the rational development and utilization of apigenin. [ABSTRACT FROM AUTHOR]

A large number of facts have shown that epigenetic modification and metabolic reprogramming represented by noncoding RNA play an important role in the invasion and metastasis of breast cancer, but the mechanism is not clear. The purpose of our study is to find a new biomarker of breast cancer and to provide a new perspective for regulating glucose metabolism and aerobic glycolysis of BC. In this paper, by downregulating C-myc protein, our team found that the expression of long-chain noncoding RNATSPAR-AS2 was significantly downregulated. However, the expression of long-chain noncoding RNASPAR-AS2 in BC is relatively high, and the prognosis is poor. TSPEAR-AS2 can promote the malignant phenotype of BC cells, including proliferation, apoptosis, invasion and metastasis, and glycolysis. At the same time, TSPEAR-AS2 can also upregulate the expression of GLUT1, an important regulator of glycolysis, thus promoting the metabolic reprogramming of BC. Molecular mechanism experiments show that TSPEAR-AS2 may promote the expression of GLUT1 by participating in IGF2BP2 modified by the GLUT1 gene. Our results suggest that the C-myc/TSPEAR-AS2/GLUT1 axis promotes the invasion and metastasis of BC by inducing glucose metabolism reprogramming. However, more phenotypic and molecular mechanism results need to be further verified. [ABSTRACT FROM AUTHOR]

Patients with high cholesterol and glucose levels are at high risk for cardiovascular disease. The Sterol Regulatory Element Binding Protein (SREBP) system regulates genes involved in lipid, cholesterol and glucose pathways. Autosomal Dominant Hypercholesterolemias (ADHs) are a group of diseases with increased cholesterol levels. They affect 1 out of every 500 individuals. About 20–30% of patients do not present any mutation in the known genes (LDLR, APOB and PCSK9). ADHs constitute a good model to identify the genes involved in the alteration of lipid levels or possible therapeutic targets. In this paper, we studied whether a mutation in the SREBP system could be responsible for ADH and other metabolic alterations present in these patients. Forty-one ADH patients without mutations in the main responsible genes were screened by direct sequencing of SREBP system genes. A luciferase reporter assay of the found mutation and an oral glucose tolerance test in carriers and non-carriers were performed. We found a novel mutation in the SREBF2 gene that increases transcription levels and cosegregates with hypercholesterolemia, and we found increased glucose levels in one family. SREBP2 is known to be involved in cholesterol synthesis, plasma levels and glucose metabolism in humans. The found mutation may involve the SREBF2 gene in hypercholesterolemia combined with hyperglycemia. [ABSTRACT FROM AUTHOR]

Chlorogenic acid compounds refer to caffeic acid quinic acid compounds, which are phenolic acid compounds synthesized by condensation of quinic acid and caffeic acid in different quantities through esterification reaction. Chlorogenic acid compounds have a variety of biological activities such as antioxidant, heat-removing and detoxifying, antibacterial and anti-inflammatory, and regulation of glucose and lipid metabolism. The paper reviews the chemical structure, main source and biological function of chlorogenic acid compounds and their application in animal husbandry production, to provide reference for further development and utilization of chlorogenic acid compounds in animal husbandry. [ABSTRACT FROM AUTHOR]

Purpose: In gestational diabetes (GDM), abnormalities occur not only in glucose metabolism, but also in lipid metabolism. Adiponectin (ADPN) plays an important role in the regulation of lipid metabolism. In this paper, the role and mechanism of ADPN in GDM are discussed. Methods: GDM model was formed in pregnant mice induced by high-fat diet and streptozotocin, and blood glucose level was detected after ADPN treatment. The levels of TG, TC, HDL-C, and LDL-C in blood lipid of mice were detected by biochemical apparatus. HE staining was used to detect the placenta damage in mice. The expression of oxidative stress-related indexes in placental tissues was also detected by ELISA. Placental iron deposition was detected by Prussian blue staining. Redox capacity of placental tissue was detected by ELISA. Western blot was used to detect the expression of ferroptosis-related proteins in placental tissues. The expression of ADPN in placenta and peripheral blood was detected by ELISA, and the expression of ADPNR, downstream CPT-1, and GLUT4 of placenta were detected by RT-qPCR and western blot. Subsequently, trophoblast cells were induced by palmitic acid and glucose, and the cell activity was detected by CCK-8. The results in animal experiments were verified in cell experiments by RT-qPCR, western blot, and fluorescence labeling of iron ions. Finally, ADPN and CPT-1 inhibitor PM were given to trophoblast cells to further explore the mechanism. Results: ADPN inhibited blood glucose and lipid levels in GDM mice. ADPN inhibited oxidation/peroxide imbalance-induced ferroptosis in placental tissues of GDM mice. ADPN inhibited the expression of CPT-1 and GLUT4 in placental tissues of GDM mice. This result was also confirmed in cell experiments, and this process may be achieved by regulating CPT-1. Conclusions: ADPN ameliorated placental injury in GDM by correcting fatty acid oxidation/peroxide imbalance-induced ferroptosis via restoration of CPT-1 activity. [ABSTRACT FROM AUTHOR]

Brain contains around one hundred and seventy-one billion cells and uses about 20% of total body energy to carry out the active function in human being. Brain is mainly dependent on Glycolysis, if the basal energy level is not maintained it can lead to synaptic loss and affect other cognitive abilities. Alzheimer's disease is a multifactorial disease that is also characterized by decreased glucose metabolism. This paper reviews about (Figure 1) the dissociation of HK from mitochondria resulting in increased IL-1β. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chongqing University of Technology (Natural Science) is the property of Chongqing University of Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Type 2 diabetes mellitus (T2DM), among other modern diseases, certainly occupies a leading position today. Moreover, the comorbid combination of T2DM and osteoarthritis (OA) is a common example of the development of complications, disability and mortality these days. As you know, T2DM develops against the background of obesity and overweight. A significant group of patients prone to these pathologies are peri- and postmenopausal women. Estrogen deficiency during this period worsens the course of these interdependent conditions. Therefore, searching for ways of early diagnosis of OA in women with T2DM is an urgent task of internal medicine. Purpose. To determine the interdependencies of indicators of glucose metabolism and lipid metabolism with levels of visfatin (VF) and homocysteine (HC) in women with T2DM and OA in peri- and postmenopause. Methods. For the study, 120 thematic women in peri- and postmenopause were selected and were divided into three groups: 1st (n = 20) -- women with a mono-course of T2DM; 2nd (n = 20) -- with a mono-course of OA; 3rd (n = 64) -- with the comorbid course of T2DM and OA. The control group (CG) consisted of 16 relatively healthy women of the appropriate age. Diagnoses of T2DM and OA were established in accordance with the current Orders of the Ministry of Health of Ukraine. Laboratory diagnostic methods were performed according to standard methods. The results. According to the obtained results, the presence of interdependencies of all indicators of lipid metabolism and glucose-insulin metabolism was reliably determined, which indicated direct correlations (mostly of moderate strength) with the levels of HC and VF in the blood of the examinees, most pronounced in the comorbid combination of T2DM and OA in peri- and postmenopause. Conclusions. In work, an analysis of the correlations of indicators of glucose metabolism and lipid metabolism with disturbances in the metabolism of VF and HC in women with T2DM and OA in pre- and postmenopause was carried out, and their interdependent relationships were determined. The highest levels of VF and HC were recorded in the group of women with comorbid pathology of T2DM and OA. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Simple Summary: The data show that long-term 150 mT SMF exposure enhanced the motility and alleviated the mental status of adult female mice by modulating glucose metabolism and gut microbiota, increasing the level of beneficial flora and antioxidant capacity. This certificated that moderate intensity long-term SMF exposure has the potential to ameliorate the locomotive and exploratory capacity and negative mood associated with female growth. Because of the high cost and safety of ultra-high magnetic resonance imaging (MRI), its application has certain limitations. Whereas 0.5–3 T MRI has been widely applied in hospitals, static magnetic fields (SMFs) have been shown to improve mice mental health and have anti-tumor potentials. Here, we compared the effects of the upward and downward 150 mT SMF groups with the sham group on C57BL/6J adult female mice. Locomotor and exploratory activity were also measured by behavioral tests, including the open field and elevated plus test. Additionally, physiology, pathology indicators and gut microbiota were examined. We found that 150 mT SMFs long-term exposure enhanced locomotive and exploratory activity of mice, especially the downward 150 mT SMF. Compared with the downward 150 mT SMF group, the movement speed and distance in the center area of the sham group were increased by 65.99% (p < 0.0001) and 68.58% (p = 0.0038), respectively. Moreover, compared to the sham group, downward 150 mT SMF increased the number of entrances to the center area by 67.0% (p = 0.0082) and time in the center area by 77.12% (p = 0.0054). Additionally, we observed that upward 150 mT SMF improved the number of follicles (~2.5 times, p = 0.0325) and uterine glands through increasing the total antioxidant capacity and reducing lipid peroxidation level in mice. Gut microbiome analysis showed that 150 mT SMFs long-term exposure improved the microbiota abundance (Clostridium, Bifidobacterium, Ralstonia and Yaniella) in the genus level, which may affect metabolism, anxiety and behavior in adult female mice. Our results demonstrated that 150 mT SMFs long-term exposure not only had good biosafety, but also improved athletic performance, emotion and the function of ovarian, uterine and gut microbiota abundance in adult female mice, which unraveled the potential of moderate long-term SMF exposure in clinical applications. [ABSTRACT FROM AUTHOR]

Au@Pt nanozyme, a bimetallic core–shell structure Au and Pt nanoparticle, has attracted significant attention due to its excellent catalytic activity and stability. Here, we propose that Au@Pt improves glucose tolerance and reduces TG after four weeks administration. The transcriptomic analysis of mouse liver tissues treated with Au@Pt nanozyme showed changes in genes related to glucose and lipid metabolism signaling pathways, including glycolysis/gluconeogenesis, pyruvate metabolism, PPAR signaling, and insulin signaling. Moreover, analysis of fecal samples from mice treated with Au@Pt nanozyme showed significant changes in the abundance of beneficial gut microbiota such as Dubosiella, Parvibacter, Enterorhabdus, Monoglobus, Lachnospiraceae_UCG-008, Lachnospiraceae_UCG-006, Lachnospiraceae_UCG-001, and Christensenellaceae_R-7_group. Combined multi-omics correlation analyses revealed that the modulation of glucose and lipid metabolism by Au@Pt was strongly correlated with changes in hepatic gene expression profiles as well as changes in gut microbial profiles. Overall, our integrated multi-omics analysis demonstrated that Au@Pt nanozyme could modulate glucose and lipid metabolism by regulating the expression of key genes in the liver and altering the composition of gut microbiota, providing new insights into the potential applications of Au@Pt nanozyme in the treatment of metabolic disorder. [ABSTRACT FROM AUTHOR]