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Clinical Diabetes 12/05/2019 16:44
Branched esters of palmitic acid and hydroxy-stearic acid (PAHSA) are anti-inflammatory and anti-diabetic lipokines that connect glucose and lipid metabolism. We aimed to characterize involvement of the 5-PAHSA regioisomer in the adaptive metabolic response of white adipose tissue (WAT) to cold exposure (CE) in mice, exploring the crosstalk between glucose utilization and lipid metabolism. CE promoted local production of 5- and 9-PAHSAs in WAT. Metabolic labeling of de novo lipogenesis (DNL) using 2 H 2 O revealed that 5-PAHSA potentiated the effects of CE and stimulated triacylglycerol/fatty acid (TAG/FA) cycling in WAT through impacting lipogenesis and lipolysis. Adipocyte lipolytic products were altered by 5-PAHSA through selective FA re.
Clinical Diabetes 11/11/2019 12:18
The ability to switch fuels for oxidation in response to changes in macronutrient composition of diet (metabolic flexibility) may be informative of the individual susceptibility to weight gain. Seventy-nine healthy, weight-stable participants underwent 24-h assessments of energy expenditure and respiratory quotient (RQ) in a whole-room calorimeter during energy balance (EBL; 50% carbohydrate, 30% fat) and then during 24-h fasting and three 200% overfeeding diets in a crossover design. Metabolic flexibility was defined as the change in 24-h RQ from EBL during fasting and standard (STOF: 50% carbohydrate, 30% fat), high-fat (HFOF: 60% fat, 20% carbohydrate), and high-carbohydrate (HCOF: 75% carbohydrate, 5% fat) overfeeding diets. Free-living.
Clinical Diabetes 11/11/2019 12:18
The whitening and loss of brown adipose tissue (BAT) during obesity and aging promote metabolic disorders and related diseases. The imbalance of Ca 2+ homeostasis accounts for the dysfunction and clearance of mitochondria during BAT whitening. Capsaicin, a dietary factor activating TRPV1, can inhibit obesity induced by high-fat diet (HFD), but whether capsaicin inhibits BAT loss and the underlying mechanism remain unclear. In this study, we determined that the inhibitory effects capsaicin on HFD-induced obesity and BAT whitening were dependent on the participation of SIRT3, a critical mitochondrial deacetylase. SIRT3 also mediated all the beneficial effects of capsaicin on alleviating ROS generation, elevating mitochondrial activity and res.
Clinical Diabetes 11/05/2019 11:21
Adipose tissue macrophages (ATMs) are involved in the development of insulin resistance in obesity. We have recently shown that myeloid cell-specific reduction of 3- hydroxy-3-methylglutaryl-coenzyme A reductase ( Hmgcr m-/m- ), which is the rate-limiting enzyme in cholesterol biosynthesis, protects against atherosclerosis by inhibiting macrophage migration in mice. We hypothesized that ATMs are harder to accumulate in Hmgcr m-/m- mice than control Hmgcr fl/fl mice in the setting of obesity. To test this hypothesis, we fed Hmgcr m-/m- and Hmgcr fl/fl mice with a high-fat diet (HFD) for 24 weeks and compared plasma glucose metabolism as well as insulin signaling and histology between the two groups. Myeloid cell-specific reduction of Hmgcr i.
Clinical Diabetes 10/25/2019 14:30
Glucagon and its partner insulin are dually linked in both their secretion from islet cells and action in the liver. Glucagon signaling increases hepatic glucose output, and hyperglucagonemia is partly responsible for the hyperglycemia in diabetes making glucagon an attractive target for therapeutic intervention. Interrupting glucagon signaling lowers blood glucose, but also results hyperglucagonemia and alpha cell hyperplasia. Investigation of the mechanism for alpha cell proliferation led to the description describe a conserved liver-alpha cell axis where glucagon is a critical regulator of amino acid homeostasis. In return, amino acids regulate alpha cell function and proliferation. New evidence suggests that dysfunction of the axis in h.
Clinical Diabetes 10/24/2019 12:36
Statins are cholesterol-lowering agents that increase the incidence of diabetes and impair glucose tolerance via their detrimental effects on nonhepatic tissues, such as pancreatic islets, but the underlying mechanism has not been determined. In atorvastatin (ator)-treated high-fat diet-fed mice, we found reduced pancreatic β-cell size and β-cell mass, fewer mature insulin granules and reduced insulin secretion and glucose tolerance. Transcriptome profiling of primary pancreatic islets showed that ator inhibited the expression of pancreatic transcription factor (TF), mTOR signaling and small G protein (sGP) genes. Supplementation of the mevalonate pathway intermediate geranylgeranyl pyrophosphate (GGPP), which is produced by 3-hydroxy-3- me.
Clinical Diabetes 10/17/2019 12:17
Insulin secretion is tightly regulated by membrane trafficking. RILP (Rab7-interacting lysosomal protein) regulates the endocytic trafficking, but its role in insulin secretion has not been investigated. In this study, we found that over-expression of RILP inhibited insulin secretion in both the β cell lines and freshly isolated islets. Consequently, the expression of RILP in islets suppressed the ability to recover the glucose homeostasis in the type 1 diabetes mice upon transplantation. Of physiological relevance is that RILP expression was up-regulated in mouse pancreas suffering from diabetes. Mechanistically, over-expression of RILP induced insulin granules clustering and a decreased number of proinsulin-containing granules in β cells,
Clinical Diabetes 10/11/2019 12:58
Adipose tissue is the key organ to coordinate whole-body energy homeostasis. Although it has been reported that ring finger protein 20 (RNF20) regulates lipid metabolism in the liver and kidney, the roles of RNF20 in adipose tissue have not been explored. Here, we demonstrate that RNF20 promotes adipogenesis by potentiating the transcriptional activity of peroxisome proliferator-activated receptor gamma (PPAR). Under normal chow diet feeding, Rnf20 defective ( Rnf20 +/– ) mice exhibited reduced fat mass with smaller adipocytes compared to wild type littermates. In addition, high-fat diet-fed Rnf20 +/– mice alleviated systemic insulin resistance accompanied by a reduced expansion of fat tissue. Quantitative proteomic analyses revealed signif.
Clinical Diabetes 10/09/2019 16:37
Abnormalities of methyl CpG-binding protein 2 (Mecp2) cause neurological disorders with metabolic dysfunction, however, its role in adipose tissues remains unclear. Here, we report upregulated Mecp2 in white adipose tissues (WAT) of obese humans, as well as in obese mice and during in vitro adipogenesis. Normal chow-fed adipocyte-specific Mecp2 knockout mice ( Mecp2 Adi KO mice) showed a lean phenotype, with downregulated lipogenic genes and upregulated thermogenic genes identified using RNA-sequencing. Consistently, deficiency of Mecp2 in adipocytes protected mice from HFD-induced obesity and inhibited in vitro adipogenesis. Furthermore, Mecp2 Adi KO mice showed increased browning under different stimuli, including cold treatment. Mechanis.
Clinical Diabetes 10/09/2019 16:37
Within the human pancreas, exocrine and endocrine cells control secretion of digestive enzymes and production of hormones to maintain metabolic homeostasis, respectively. While the vast majority of type 1 diabetes research efforts have focused on endocrine function and autoimmunity, recent studies identified a series of unique features (e.g., reduced weight and volume, increased density of leukocytes) within the exocrine pancreas in this disease, but the mechanisms underlying these aberrancies are unknown. Therefore, we histologically assessed amylase, insulin, glucagon, lipase and/or trypsinogen in 78 organ donor pancreata, from birth through adulthood in controls and those at various stages of type 1 diabetes. While amylase-positive acina.
Clinical Diabetes 10/03/2019 13:25
Novel biomarkers of type 2 diabetes (T2D) and response to preventative treatment in individuals with similar clinical risk may highlight metabolic pathways that are important in disease development. We profiled 331 metabolites in 2,015 baseline plasma samples from the Diabetes Prevention Program (DPP). Cox models were used to determine associations between metabolites and incident T2D, as well as whether associations differed by treatment group (i.e. lifestyle (ILS), metformin (MET), or placebo (PLA)) over an average of 3.2 years of follow up. We found 69 metabolites associated with incident T2D regardless of treatment randomization. In particular, cytosine was novel and associated with the lowest risk. In an exploratory analysis, 35 baseli.
Clinical Diabetes 09/16/2019 22:13
Melanin concentrating hormone (MCH) is an important regulator of food intake, glucose metabolism and adiposity. However, the mechanisms mediating these actions remain largely unknown. We used pharmacological and genetic approaches to show that the SIRT1/FoxO1 signaling pathway in the hypothalamic arcuate nucleus (ARC) mediates MCH-induced feeding, adiposity and glucose intolerance. MCH reduces POMC neuronal activity and the SIRT1/FoxO1 pathway regulates the inhibitory effect of MCH on POMC expression. Remarkably, the metabolic actions of MCH are compromised in mice lacking SIRT1 specifically in POMC neurons. Of note, the actions of MCH are independent of AgRP neurons because inhibition of GABA-R in the ARC did not prevent the orexigenic act.
Clinical Diabetes 09/13/2019 15:16
Reduction of β-cell mass and function is central to the pathogenesis of type 2 diabetes. The terms glucotoxicity, lipotoxicity, and glucolipotoxicity are used to describe potentially responsible processes. The premise is that chronically elevated glucose levels are toxic to β-cells, that elevated lipid levels in the form of circulating free fatty acids (FFA) also have toxic effects, and that the combination of the two, glucolipotoxicity, is particularly harmful. Much work has shown that high concentrations of FFA can be very damaging to β-cells when used for in vitro experiments, and when infused in large amounts in humans and rodents they produce suppression of insulin secretion. The purpose of this Perspective is to raise doubts about whe.
Clinical Diabetes 09/13/2019 15:16
Inactivation of the β cell transcription factor NEUROD1 causes diabetes in mice and humans. In this study, we uncovered novel functions of Neurod1 during murine islet cell development and during the differentiation of human embryonic stem cells (HESCs) into insulin-producing cells. In mice, we determined that Neurod1 is required for perinatal proliferation of alpha and beta cells. Surprisingly, apoptosis only makes a minor contribution to beta cell loss when Neurod1 is deleted. Inactivation of NEUROD1 in HESCs severely impaired their differentiation from pancreatic progenitors into insulin expressing (HESC-beta) cells; however survival or proliferation was not affected at the time points analyzed. NEUROD1 was also required in HESC-beta cell.
Clinical Diabetes 09/10/2019 16:25
Extreme obesity (EO, BMI>50) is frequently associated with neuropsychiatric disease (NPD). As both EO and NPD are heritable central nervous system disorders, we assessed the prevalence of protein truncating (PTV) and copy number variants (CNV) in genes/regions previously implicated in NPD, in adults with EO (n=149) referred for weight loss/bariatric surgery. We also assessed the prevalence of CNVs in patients referred to University College London Hospital (UCLH) with EO (n=218) and obesity (O, BMI 35-50, n=374) and a Swedish cohort of participants from the community with predominantly O (n=161). The prevalence of variants was compared to controls in ExAC/gnomAd database. In the discovery cohort (high NPD prevalence: 77%), the cumulative PTV.
Clinical Diabetes 09/06/2019 15:01
While peripheral neuropathy is the most common complication of long-term diabetes, cognitive deficits associated with encephalopathy and myelopathy also occur. Diabetes is a risk factor for Alzheimer’s disease (AD) and increases risk of progression from mild cognitive impairment to AD. The only current recommendation for preventing or slowing progression of peripheral neuropathy is to maintain close glycemic control, while there is no recommendation for CNS disorders. NSI-189 is a new chemical entity that when orally administered promotes neurogenesis in the adult hippocampus, increases hippocampal volume, enhances synaptic plasticity and reduces cognitive dysfunction. To establish the potential for impact on peripheral neuropathy, we first.
Clinical Diabetes 09/06/2019 15:01
Obesity-related insulin resistance (IR) may develop in multiple organs, representing different etiologies towards cardiometabolic diseases. We identified abdominal subcutaneous adipose tissue (ScAT) transcriptome profiles in relation to liver or muscle IR by means of RNA sequencing in overweight/obese participants of the DiOGenes cohort (n=368). Tissue-specific IR phenotypes were derived from a 5-point oral glucose tolerance test. Hepatic and muscle IR were characterized by distinct abdominal ScAT transcriptome profiles. Genes related to extracellular remodeling were upregulated in individuals with primarily hepatic IR, whilst genes related to inflammation were upregulated in individuals with primarily muscle IR. In line with this, in two i.

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