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BACKGROUND: Lead (Pb) is an ancient toxic metal and is still a major public health issue. Our previous study found that Pb exposure promotes metabolic disorders in obese mice, but the molecular mechanisms remain unclear. The present study explored the effects of Pb exposure on glucose homeostasis in mice fed a normal diet (ND) and high-fat diet (HFD) from the perspective of gut microbiota. RESULTS: Pb exposure had little effect on glucose metabolism in ND mice, but exacerbated hyperglycemia and insulin resistance, and impaired glucose tolerance in HFD mice. Pb exposure impaired intestinal tight junctions and mucin expression in HFD mice, increasing intestinal permeability and inflammation. Moreover, Pb exposure altered the composition and structure of the gut microbiota and decreased short-chain fatty acids (SCFAs) levels in HFD mice. Correlation analysis revealed that the gut microbiota and SCFAs were significantly correlated with the gut barrier and glucose homeostasis. Furthermore, the fecal microbiota transplantation from Pb-exposed HFD mice resulted in glucose homeostasis imbalance, intestinal mucosal structural damage and inflammation in recipient mice. However, Pb did not exacerbate the metabolic toxicity in HFD mice under depleted gut microbiota. CONCLUSION: The findings of the present study suggest that Pb induces impairment of glucose metabolism in HFD mice by perturbing the gut microbiota. Our study offers new perspectives on the mechanisms of metabolic toxicity of heavy metals and demonstrates that the gut microbiota may be a target of action for heavy metal exposure. [ABSTRACT FROM AUTHOR]

Aronia melanocarpa fruit contains a variety of active ingredients, such as phenolic acids, anthocyanins, proanthocyanidins, etc. Relevant in vivo and in vitro studies have concluded that it has beneficial effects in terms of treating dyslipidemia, hypertension, glucose metabolism disorders, etc. This article discusses the nutritional value and food processing of Aronia melanocarpa and reviews the chemical components of Aronia melanocarpa and the pharmacological activities of related substances in order to summarize the chemical characteristics of the fruit and its development prospects. The process optimization of juice production, the impact of antioxidant capacity, and the comprehensive utilization of pomace in feed are discussed. This article provides a reference for future comprehensive application research and product development of Aronia melanocarpa. [ABSTRACT FROM AUTHOR]

Maintaining blood glucose at an appropriate physiological level requires precise coordination of multiple organs and tissues. The vagus nerve bidirectionally connects the central nervous system with peripheral organs crucial to glucose mobilization, nutrient storage, and food absorption, thereby presenting a key pathway for the central control of blood glucose levels. However, the precise mechanisms by which vagal populations that target discrete tissues participate in glucoregulation are much less clear. Here we review recent advances unraveling the cellular identity, neuroanatomical organization, and functional contributions of both vagal efferents and vagal afferents in the control of systemic glucose metabolism. We focus on their involvement in relaying glucoregulatory cues from the brain to peripheral tissues, particularly the pancreatic islet, and by sensing and transmitting incoming signals from ingested food to the brain. These recent findings - largely driven by advances in viral approaches, RNA sequencing, and cell-type selective manipulations and tracings - have begun to clarify the precise vagal neuron populations involved in the central coordination of glucose levels, and raise interesting new possibilities for the treatment of glucose metabolism disorders such as diabetes. [ABSTRACT FROM AUTHOR]

Background: Alisol A can ameliorate glucose metabolism disorders, however, there is no data regarding its role in diabetic nephropathy (DN). The present work evaluates the role of Alisol A in DN and the underlying mechanism. Methods: RNA expression of circ_0001831, miR‐346, and lin‐28 homolog B (LIN28B) was detected by qRT‐PCR. Cell viability and proliferation were investigated by MTT assay and EdU assay, respectively. The inflammatory cytokines were examined by ELISAs. Oxidative stress was evaluated by the commercial kits. Protein expression was detected by western blotting. The interactions among circ_0001831, miR‐346, and LIN28B were identified by dual‐luciferase reporter assay and RIP assay. DN mouse model assay was used to analyse the effect of Alisol A on renal injury of diabetic mice. Results: HG treatment promoted HRMC proliferation, fibrosis, inflammation, and oxidative stress; however, these effects were reversed after Alisol A treatment. Alisol A treatment ameliorated STZ‐induced renal injury of diabetic mice. Additionally, circ_0001831 or LIN28B overexpression or miR‐346 downregulation relieved Alisol A‐induced effects under HG conditions. Mechanistically, circ_0001831 acted as a miR‐346 sponge, and LIN28B was identified as a target gene of miR‐346. Further, the regulation of circ_0001831 in HG‐induced HRMC dysfunction involved LIN28B. Conclusion: Alisol A ameliorated HG‐induced HRMC fibrosis, inflammation, and oxidative stress and STZ‐induced renal injury of diabetic mice by regulating the circ_0001831/miR‐346/LIN28B pathway. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is a metabolic inflammatory disease with a high incidence worldwide. Patients with DM are at a high risk for all types of infections. Type 1 DM is characterised with immune destruction of pancreatic β cells, while type 2 diabetes is characterised with insulin resistance and β cell dysfunction, both of which result in disorders of glucose and lipid metabolism. This metabolic disorder causes functional defects of immune cells, aberrant production of inflammatory cytokines, dysregulated immune responses, advanced pathophysiological injury of the body, and increased mortality in populations with DM upon infections. Starting with the change of natural immune system in patients with DM, this paper focused on the enhanced severity of infections in DM and the underlying innate immune alterations in preclinical and clinical studies, aiming to better understand the influence of DM on the susceptibility, pathophysiology, and clinical outcomes in infections. [ABSTRACT FROM AUTHOR]

Introduction: Treatment strategies for depression based on interventions for glucose and lipid metabolism disorders are receiving increasing attention. Investigating the mechanism of their antidepressant effect and exploring new diagnostic and therapeutic biomarkers have attracted increasing attention. Dulaglutide, a long‐acting GLP‐1 receptor agonist, has been reported to alleviate cognitive deficits and neuronal damage. However, the antidepressant effect of dulaglutide and, especially, the underlying mechanism are still poorly understood. In this study, we aimed to explore the underlying biomarkers of depression and potential modulatory targets of dulaglutide in chronic mild stress (CMS) mice. Methods: Sixty mice were randomly divided into a control group (CON group), a CMS+Vehicle group (CMS+Veh group), a CMS+0.3 mg/kg dulaglutide group (Low Dula group), and a CMS+0.6 mg/kg dulaglutide group (High Dula group). Numerous behavioral tests, mainly the open field test, forced swimming test, and tail suspension test, were applied to evaluate the potential effect of dulaglutide treatment on anxiety‐ and depression‐like behaviors in mice exposed to chronic stress. Furthermore, a liquid chromatography–tandem mass spectrometry‐based metabolomics approach was utilized to investigate the associated mechanisms of dulaglutide treatment. Results: Three weeks of dulaglutide treatment significantly reversed depressive‐like but not anxiety‐like behaviors in mice exposed to chronic stress for 4 weeks. The results from the metabolomics analysis showed that a total of 20 differentially expressed metabolites were identified between the CON and CMS+Veh groups, and 46 metabolites were selected between the CMS+Veh and High Dula groups in the hippocampus of the mice. Comprehensive analysis indicated that lipid metabolism, amino acid metabolism, energy metabolism, and tryptophan metabolism were disrupted in model mice that experienced depression and underwent dulaglutide therapy. Conclusion: The antidepressant effects of dulaglutide in a CMS depression model were confirmed. We identified 64 different metabolites and four major pathways associated with metabolic pathophysiological processes. These primary data provide a new perspective for understanding the antidepressant‐like effects of dulaglutide and may facilitate the use of dulaglutide as a potential therapeutic strategy for depression. [ABSTRACT FROM AUTHOR]

Objective: Children born small for gestational age (SGA) are at a greater risk of developing insulin resistance, type 2 diabetes, and cardiovascular disease in adulthood. Gastrointestinal peptides, some secreted by intestinal L cells, regulate glucose and lipid metabolism and act on the hypothalamus to regulate energy homeostasis. The aim of this study was to explore whether gastrointestinal peptides are involved in metabolic disorders in SGA, which remains unclear. Methods: The secretion of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) were investigated in prepubertal children born SGA, the differences between catch-up growth and persistent short stature were compared, and correlation with glucose and lipid metabolism was analyzed. GLP-1, PYY, insulin-like growth factor 1, glucose, insulin, and lipid concentrations were analyzed in prepubertal children aged 4-10 years, stratified into three groups: short-SGA (SGA-s), catch-up growth SGA, and normal growth appropriate for gestational age (AGA). Results: Fasting GLP-1 and PYY concentrations were significantly lower in the SGA group than in the AGA group (p<0.05), and the GLP-1 level in infants born SGA with catch-up growth was lower than that in the SGA-s group (p<0.05). In the SGA population, GLP-1 showed a weak negative correlation with catch-up growth (r=-0.326) and positive correlation with fasting insulin (r=0.331). Conclusion: Lower GLP-1 concentrations may be associated with abnormal glucose metabolism in prepubertal children born SGA with catch-up growth. This is indirect evidence that impaired intestinal L cell function may be involved in the development of metabolic complications in SGA children. [ABSTRACT FROM AUTHOR]

Introduction: The purpose of this study was to compare the difference in abdominal fat distribution between different metabolic groups and find the ectopic fat with the most risk significance. Methods: A total of 98 subjects were enrolled; there were 53 cases in the normal glucose metabolism group and 45 cases in the abnormal glucose metabolism group. Chemical shift-encoded magnetic resonance imaging was applied for quantification of pancreatic fat fraction (PFF) and hepatic fat fraction (HFF), subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT). The correlation and the difference of fat distribution between different metabolism groups were analyzed. The receiver operating characteristic (ROC) curve was used to analyze the suggestive effect of different body fat fraction. Results: Correlation analysis showed that body mass index (BMI) had the strongest correlation with fasting insulin (r = 0.473, p < 0.001), HOMA-IR (r = 0.363, p < 0.001), and C-reactive protein (r = 0.245, p < 0.05). Pancreatic fat has a good correlation with fasting blood glucose (r = 0.247, p < 0.05) and HbA1c (r = 0.363, p < 0.001). With the increase of BMI, PFF, VAT, and SAT showed a clear upward trend, but liver fat was distributed relatively more randomly. The pancreatic fat content in the abnormal glucose metabolism group is significantly higher than that in the normal group, and pancreatic fat is also a reliable indicator of abnormal glucose metabolism, especially in the normal and overweight groups (the area under the curve was 0.859 and 0.864, respectively). Conclusion: MR-based fat quantification techniques can provide additional information on fat distribution. There are differences in fat distribution among people with different metabolic status. People with more severe pancreatic fat deposition have a higher risk of glucose metabolism disorders. [ABSTRACT FROM AUTHOR]

Endothelial damage caused by persistent glucose and lipid metabolism disorders is the main reason of diabetic vascular diseases. Daidzein exerts positive effects on vascular dysfunction. Peroxisome proliferator-activated receptors (PPARs) regulate critically glucose and lipid metabolism. However, the interaction of daidzein to PPARs is still insufficiently explored. In this study, the cell proliferation was detected by EdU. The intrinsic activity and binding affinity of daidzein for human PPARs (hPPARs) were estimated by transactivation reporter gene test and HPLC-UV method, respectively. Daidzein significantly reversed high glucose (HG, at 30 mmol/l)-induced injury in HUVECs, which was inhibited by both PPARα and PPARγ antagonist, but no PPARβ antagonist. Daidzein selectively activated hPPARα and hPPARγ1, but weakly hPPARβ. Additionally, daidzein also bound to both hPPARα and hPPARγ1. The findings suggested that daidzein may be a PPARα and PPARγ dual-agonist. The amelioration of daidzein on HUVECs from hyperglycemia may be mediated by the activation of PPARα and PPARγ receptors. [ABSTRACT FROM AUTHOR]

The hepatokine leukocyte cell-derived chemotaxin-2 (LECT2) promotes insulin resistance and hepatic fibrogenesis. In rodents, acute exercise suppresses circulating LECT2; however, human data are lacking. This study compared circulating LECT2 across populations and explored whether acute exercise impacts circulating LECT2. In Part A (n = 43), data were pooled from three experimental studies, regarding the following groups: healthy individuals, individuals with impaired glycaemic regulation (IGR), and individuals with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease (T2DM-MASLD). Generalised linear models assessed differences in circulating LECT2 among groups. Part B (n = 20) involved exercise (30 min, 65% peak oxygen uptake) and control (resting) trials in the healthy and IGR groups. Circulating LECT2 was measured before and at 0, 1, 2 and 3 h post-exercise. Generalised estimating equations assessed differences in LECT2 responses to the trials among groups. In Part A, circulating LECT2 levels were 28.7% and 37.3% higher in the IGR and T2DM-MASLD groups, vs. healthy individuals (p ≤ 0.038), with BMI identified as the main predictor (p = 0.008). In Part B, average circulating LECT2 levels were 6.3% higher after exercise vs. in the control (p < 0.001), with similar responses between groups (p = 0.829). In the combined cohort, circulating LECT2 levels were elevated 1–3 h after exercise vs. control (p ≤ 0.009). LECT2 is elevated in people with dysglycaemia, with BMI as a leading predictor. Contrary to previous rodent work, acute exercise augments, rather than suppresses, circulating LECT2 in humans. [ABSTRACT FROM AUTHOR]

G protein-coupled receptors (GPCRs) are a large family of membrane protein receptors, and Takeda G protein-coupled receptor 5 (TGR5) is a member of this family. As a membrane receptor, TGR5 is widely distributed in different parts of the human body and plays a vital role in regulating metabolism, including the processes of energy consumption, weight loss and blood glucose homeostasis. Recent studies have shown that TGR5 plays an important role in glucose and lipid metabolism disorders such as fatty liver, obesity and diabetes. With the global obesity situation becoming more and more serious, a comprehensive explanation of the mechanism of TGR5 and filling the gaps in knowledge concerning clinical ligand drugs are urgently needed. In this review, we mainly explain the anti-obesity mechanism of TGR5 to promote the further study of this target, and show the electron microscope structure of TGR5 and review recent studies on TGR5 ligands to illustrate the specific binding between TGR5 receptor binding sites and ligands, which can effectively provide new ideas for ligand research and promote drug research. TGR5 can serve as an effective target for the treatment of obesity by regulating thermogenesis, metabolism, inflammation and appetite. [Display omitted] [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare 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 pathogenesis of diabetes is accompanied by increased levels of inflammatory factors, also known as "metabolic inflammation", which runs through the whole process of the occurrence and development of the disease. Mitochondria, as the key site of glucose and lipid metabolism, is often accompanied by mitochondrial function damage in type 2 diabetes mellitus (T2DM). Damaged mitochondria release pro‐inflammatory factors through damage‐related molecular patterns that activate inflammation pathways and reactions to oxidative stress, further aggravate metabolic disorders, and form a vicious circle. Currently, the pathogenesis of diabetes is still unclear, and clinical treatment focuses primarily on symptomatic intervention of the internal environment of disorders of glucose and lipid metabolism with limited clinical efficacy. The proinflammatory effect of mitochondrial damage‐associated molecular pattern (mtDAMP) in T2DM provides a new research direction for exploring the pathogenesis and intervention targets of T2DM. Therefore, this review covers the most recent findings on the molecular mechanism and related signalling cascades of inflammation caused by mtDAMP in T2DM and discusses its pathogenic role of it in the pathological process of T2DM to search potential intervention targets. [ABSTRACT FROM AUTHOR]

Simple Summary: Glucose metabolism was the first metabolic pathway to be discovered and serves a central role across all life by generating energy. Cancer cells hijack glycolysis to promote growth and metastasis. Understanding the molecular basis of glycolytic rewiring in cancers could illuminate new treatment approaches. Glycolysis is the central metabolic pathway across all kingdoms of life. Intensive research efforts have been devoted to understanding the tightly orchestrated processes of converting glucose into energy in health and disease. Our review highlights the advances in knowledge of how metabolic and gene networks are integrated through the precise spatiotemporal compartmentalization of rate-limiting enzymes. We provide an overview of technically innovative approaches that have been applied to study phosphofructokinase-1 (PFK1), which represents the fate-determining step of oxidative glucose metabolism. Specifically, we discuss fast-acting chemical biology and optogenetic tools that have delineated new links between metabolite fluxes and transcriptional reprogramming, which operate together to enact tissue-specific processes. Finally, we discuss how recent paradigm-shifting insights into the fundamental basis of glycolytic regulatory control have shed light on the mechanisms of tumorigenesis and could provide insight into new therapeutic vulnerabilities in cancer. [ABSTRACT FROM AUTHOR]

Copyright of Forum Zaburzen Metabolicznych is the property of VM Medica-VM Group (Via Medica) 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.)

Introduction: Visfatin and nesfatin are active proteins that are involved in the regulation of physiological functions such as glucose metabolism and inflammatory response. This study aimed to assess the influence of visfatins and nystatins gene variants on the occurrence of the full metabolic syndrome or its components. Material and methods: The research cohort comprised 285 diabetic patients, 132 men and 153 women. Specific DNA segments were amplified and labelled, and the rs 4730153 gene of visfatin and the rs 1330 gene of nesfatin were analysed. Real-Time PCR was conducted using fluorescence-labelled probes. Results: The AA genotype of visfatin (rs 4730153) shows a positive association with glucose concentration or pharmacological treatment in patients with type 2 diabetes, compared to AG and GG genotypes. The GG genotype of nesfatin (rs 1330) shows a positive association with incidents of metabolic syndrome, compared to the AA genotype. Conclusions: Visfatin polymorphism in rs 4730153 may be associated with inappropriate glucose concentration. Nesfatin polymorphism in rs 1330 may be associated with metabolic syndrome. Further studies in a larger group of patients are necessary to completely assess this association. [ABSTRACT FROM AUTHOR]

This document is an editorial published in Frontiers in Endocrinology titled "The relationship between diabetes and cancers and its underlying mechanisms, volume II." The editorial discusses the potential relationship between diabetes mellitus (DM) and cancer morbidity or mortality. It highlights studies that have found a higher risk of developing oral cancer and potentially malignant disorders in patients with DM, as well as the association between DM and hepatocellular carcinoma. The editorial emphasizes the need for clinical trials in humans to further understand the roles of diabetes in cancer development and the importance of cancer screening in patients with DM. [Extracted from the article]

Diabetes mellitus (DM) is now regard as a worldwide health issue affecting hundreds millions of people. It is a metabolic disease targeting glucose metabolism and insulin homeostasis, Type 2 diabetes mellitus (T2DM) is the most prevent type of this disease accounting about 90-95% of the disease as whole. microRNAs (miRNAs) which are a small non-coding RNAs, they revolutionized as potential new biomarkers for the diagnosis and prognosis of a wide range of disorders. Recent studies prove the relationship between miR-21 and inflammatory process and insulin resistance, our emphasis suggest there is a role of miR-21 in insulin resistance in T2DM. Studies have explored the potential of miR-21 as diagnostic biomarkers for T2DM. The purpose of this study is to compare the sera levels of miRNA-21 among newly diagnosed patients e with T2DM patients with their levels in apparently healthy subjects using blood samples. The time frame for this case-control research is August 2022 through March 2023, and it took place at Al-Sadr Teaching Hospital/Masin / Iraq. There were 100 patients home recent diagnosed with T2DM (50 females and 50 males) with age ranged between (20 -70 years) and 100 apparently healthy subject who dealt with as control group. 2 ml of blood drown from each patient and healthy person, putted it in EDTA tube with 1 ml of Trizole as a preservative, and put the tubes in the freezer at -70 degrees Celsius until analyze the samples. [ABSTRACT FROM AUTHOR]

BACKGROUND. Glucose metabolism disorders (GMD) were detected both in acute and in post-COVID, however, its pathogenic aspects remain unclear.AIM. To analyze the occurrence of GMD in post-COVID patients who have had moderate and severe COVID-19 without previously known GMD disorders, and evaluate expression of SARS-CoV-2 proteins and its entry factors in pancreas in acute COVID-19.METHODS. Among 187 hospitalized patients with confirmed COVID-19 141 patients without previously diagnosed GMD underwent follow-up post-COVID visits. The examination for all patients included anthropometric measurement with calculation of BMI, level of HbA1c and fasting plasma glucose, for 106 patients level of insulin and HOMA-IR index was analyzed. For histological examination, pancreas fragments of 20 patients with fatal outcome were selected. Immunohistochemical study was performed with antibodies to SARS-CoV-2, ACE2, DPP4, as well as double-labeled immunofluorescence microscopy (insulin-SARS-CoV-2, insulin-ACE2, insulin-DPP4).RESULTS. Among 141 patients in post-COVID period, 9 (6.3%) had HbA1c or fasting plasma glucose levels that met criteria for diabetes mellitus, 38 (26.9%) — exceeded normal values (WHO), and 84 (59.6%) had GMD according to criteria of the ADA. In post-COVID, patients with GMD had a higher BMI and HOMA-IR index (p=0.001) compared to patients with normal glycemic levels. Only 40.4% of people had HOMA-IR index above 2.7. Patients with GMD had higher level of CRP (p=0.007) and a maximum glucose level (p=0.019) in the acute period. Positive relationship was found between BMI and HOMA index both in acute (p

To analyze the relationship between intestinal flora and glucose metabolism changes in CGIUGR rats by interventing CG-IUGR rats with the intestinal flora of normal rats. Methods SD rats were divided into three groups: the control group, the CG-IUGR group and the CG-IUGR+intestinal bacteria group (n=8 in each group). The CG IUGR rat model was established by low-calorie diet. The intestinal flora of rats in the control group were transplanted into CG-IUGR rats in the CG-IUGR+intestinal bacteria group at 3-week-old (once a week, 6 times in total). From birth to 8 weeks, the body weight and body length were measured in three groups of rats, and body mass index (BMI) was calculated. The relevant indexes of glucose metabolism were detected in three groups, including fasting blood glucose (FBG), serum fasting insulin (FINS) and serum insulin (INS) at 15 min after glucose loading and tolerance test of glucose and insulin. The mRNA and protein expression levels of skeletal muscle glycogen synthase (GYS)1 and liver GYS2 were detected by realtime fluorescence quantitative polymerase chain reaction (qPCR) and Western blot assay respectively. The activities of GYS in skeletal muscle and liver were detected. 16S rDNA sequencing was used to detect the diversity and composition of intestinal flora in rats of three groups. Results Compared with the control group, the body length, body weight and BMI of rats in the CG-IUGR group were all increased significantly during the process of growth and development. Its serum FINS level decreased, and serum FBG had no significant change. The blood glucose levels of rats in the CG-IUGR group were significantly up-regulated after glucose and INS loading. The serum INS level of rats in the CG-IUGR group was significantly up-regulated at 15 min after glucose loading. The mRNA and protein expression levels of skeletal muscle GYS1 and liver GYS2 in rats of the CG-IUGR group were decreased, and the activity of GYS was also decreased (P＜0.05). These above changes of rats in the CG-IUGR+intestinal bacteria group were all improved (P＜0.05). Compared with the control group, ACE and Chao1 indices of intestinal bacteria in rats of the CG-IUGR group were lower (P＜0.05). Compared with the CG-IUGR group, the relative abundance of intestinal bifidobacterium in rats of the CG-IUGR+intestinal bacteria group was increased (P＜0.05). Conclusion IUGR can attenuate the glucose metabolism fuction of CG-IUGR rats by downregulating the expression and activity of GYS in skeletal muscle and liver tissue. The abnormal glucose metabolism in CGIUGR rats is related to changes of intestinal flora. [ABSTRACT FROM AUTHOR]