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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 09/10/2019 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
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.
Clinical Diabetes 08/22/2019 17:43
The contribution of the sympathetic (SNS) versus parasympathetic (PSNS) nervous system in mediating fatal cardiac arrhythmias during insulin-induced severe hypoglycemia is not well understood. Therefore, experimental protocols were performed in non-diabetic, Sprague Dawley rats to test SNS with 1) adrenal demedullation and 2) chemical sympathectomy, and to test PSNS with 3) surgical vagotomy, 4) nicotinic receptor (mecamylamine) and muscarinic receptor (AQ-RA 741) blockade, and 5) ex vivo heart perfusions with normal or low glucose, acetylcholine and/or mecamylamine. In protocols 1-4, 3-hour hyperinsulinemic (0.2U·kg –1 ·min –1 )-hypoglycemic (10-15 mg/dl) clamps were performed. Adrenal demedullation and chemical sympathectomy had no effect.
Clinical Diabetes 08/09/2019 17:08
CGM readings are delayed relative to blood glucose, and this delay is usually attributed to the latency of interstitial glucose levels. However, CGM-independent data suggest rapid equilibration of interstitial glucose. This study seeks to determine the loci of CGM delays. Electrical current was measured directly from CGM electrodes to define sensor kinetics in the absence of smoothing algorithms. CGMs were implanted in mice, and sensor versus blood glucose responses were measured following an intravenous glucose challenge. Dispersion of a fluorescent glucose analogue (2-NBDG) into the CGM micro-environment was observed in vivo using intravital microscopy. Tissue deposited on the sensor and non-implanted subcutaneous adipose tissue were then.
Clinical Diabetes 08/09/2019 17:08
We examined the relationship between insulin clearance, insulin sensitivity and β -cell function and the longitudinal effect of insulin clearance on β -cell function in lean, obese insulin sensitive and insulin resistant adolescents. A hyperinsulinemic-euglycemic and a hyperglycemic clamp were performed in 110 youths to quantify hepatic and peripheral clearance, insulin sensitivity and β-cell function (disposition index, DI h-clamp ).
Clinical Diabetes 07/15/2019 10:00
IN BRIEF To be consistently effective, insulin must be delivered into subcutaneous tissue. If insulin is delivered intramuscularly, its uptake and action become variably faster, leading to suboptimal, inconsistent glucose control. The best strategy to avoid intramuscular injection is to use the shortest needles available. Injection sites should be rotated systematically to prevent lipohypertrophy, which also substantially affects insulin uptake and action. New evidence-based insulin delivery recommendations are available, and awareness of them should lead to more effective use of insulin therapy, improved clinical outcomes, and considerable cost savings.
Clinical Diabetes 06/14/2019 16:13
Exogenous ghrelin reduces glucose-stimulated insulin secretion and endogenous ghrelin protects against hypoglycemia during starvation. Islet -cells produce ghrelin and -cells express growth hormone secretagogue receptor (GHSR), suggestion the possibility of a paracrine mechanism for islet ghrelin to reach high local concentrations and affect insulin secretion. GHSR has high constitutive activity and may act independently of ghrelin. The objective in this study was to determine whether an intra-islet ghrelin-GHSR axis modulates insulin secretion and glucose metabolism using mouse models lacking ghrelin ( Ghrl -/- ) or GHSR ( GHSR -/- ). GHSR -/- and GHSR +/+ mice had comparable islet ghrelin concentrations. Exogenous ghrelin decreased insuli.
Clinical Diabetes 06/14/2019 16:13
Transcription factors positively and/or negatively impact gene expression by recruiting coregulatory factors, which interact through protein-protein binding. Here we demonstrate that mouse pancreas size and islet β cell function are controlled by the ATP-dependent Swi/Snf chromatin remodeling coregulatory complex that physically associates with Pdx1, a diabetes-linked transcription factor essential to pancreatic morphogenesis and adult islet-cell function and maintenance. Early embryonic deletion of just the Swi/Snf Brg1 ATPase subunit reduced multipotent pancreatic progenitor cell proliferation and resulted in pancreas hypoplasia. In contrast, removal of both Swi/Snf ATPase subunits, Brg1 and Brm, was necessary to compromise adult islet β
Clinical Diabetes 06/06/2019 14:01
Fatty Acid Binding Protein 4 (FABP4) is a leaderless lipid carrier protein primarily expressed by adipocytes and macrophages that not only functions intracellularly but is also secreted. The secretion is mediated via unconventional mechanism(s) and in a variety of species, metabolic dysfunction is correlated with elevated circulating FABP4 levels. In diabetic animals, neutralizing antibodies targeting serum FABP4 increase insulin sensitivity and attenuate hepatic glucose output suggesting the functional importance of circulating FABP4. Using animal and cell-based models, we show that FABP4 is secreted from white, but not brown, adipose tissue in response to lipolytic stimulation in a Sirtuin-1 (SIRT1) dependent manner via a mechanism that r.
Clinical Diabetes 05/15/2019 10:00
Although insulin resistance consistently occurs with type 1 diabetes, its predominant driver is uncertain. We therefore determined the relative contributions of hyperglycemia and iatrogenic hyperinsulinemia to insulin resistance using hyperinsulinemic-euglycemic clamps in three participant groups (n=10/group) with differing insulinemia and glycemia: healthy controls (euinsulinemia, euglycemia), glucokinase maturity-onset of the young (GCK-MODY; euinsulinemia, hyperglycemia), and type 1 diabetes (hyperinsulinemia, hyperglycemia matching GCK-MODY). We assessed the contribution of hyperglycemia by comparing insulin sensitivity in control and GCK-MODY and the contribution of hyperinsulinemia by comparing GCK-MODY and type 1 diabetes. HbA1c was
Clinical Diabetes 05/15/2019 10:00
Hyperglycemia-triggered vascular abnormalities are the most serious complications of diabetes mellitus (DM). The major cause of vascular dysfunction in DM is endothelial injury and dysfunction associated with the reduced number and dysfunction of endothelial progenitor cells (EPCs). A major challenge is to identify key regulators of EPCs to restore DM-associated vascular dysfunction. Here, we show that EPCs from heterozygous knockout Aggf1 +/- mice showed impairment of proliferation, migration, angiogenesis, and transendothelial migration as in hyperglycemic mice fed with a high fat diet (HFD) or db/db mice. The number of EPCs from Aggf1 +/- mice was significantly reduced. Ex vivo , AGGF1 protein can fully reverse all damaging effects of hy.

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