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Ghrelin exerts key effects on islet hormone secretion to regulate blood glucose levels. Here, we sought to determine whether ghrelin's effects on islets extend to the alteration of islet size and [beta] cell mass. We demonstrate that reducing ghrelin - by ghrelin gene knockout (GKO), conditional ghrelin cell ablation, or high-fat diet (HFD) feeding - was associated with increased mean islet size (up to 62%), percentage of large islets (up to 854%), and [beta] cell cross-sectional area (up to 51%). In GKO mice, these effects were more apparent in 10- to 12-week-old mice than in 4-week-old mice. Higher [beta] cell numbers from decreased [beta] cell apoptosis drove the increase in [beta] cell cross-sectional area. Conditional ghrelin cell ablation in adult mice increased the [beta] cell number per islet by 40% within 4 weeks. A negative correlation between islet size and plasma ghrelin in HFD-fed plus chow-fed WT mice, together with even larger islet sizes in HFD-fed GKO mice than in HFD-fed WT mice, suggests that reduced ghrelin was not solely responsible for diet-induced obesity-associated islet enlargement. Single-cell transcriptomics revealed changes in gene expression in several GKO islet cell types, including upregulation of Manf, Dnajc3, and Gnas expression in [beta] cells, which supports decreased [beta] cell apoptosis and/or increased [beta] cell proliferation. These effects of ghrelin reduction on islet morphology might prove useful when designing new therapies for diabetes., Introduction Ghrelin is secreted primarily by gastric ghrelin cells (1). It is mainly via binding to CNS and pituitary growth hormone secretagogue receptors (GHSRs) that ghrelin's actions to increase GH [...]

The transition in eating behaviour toward a diet rich in calories and low in vegetables is a major factor responsible for the rapid increase in the incidence of obesity and diabetes. The research aimed at investigating the effect of a high-calorie diet and vegetables on feeding behaviour, weight gain and blood sugar in male Wistar rats. The vegetables were dried, blended, and preserved in airtight containers. Thirty male Wistar rats weighing an average of 127.4 g were housed in 6 cages with 5 rats in each cage. There were six groups comprising the positive control which was fed standard rat feed and water, also the negative control which was given a high-calorie diet (high-fat feed and sugar water) and four treatment groups. The four treatment groups were fed on a high-calorie diet with a 5 % concentration of either Corchorus olitorius, Crassocephalum crepidiodes, Amaranthus hybridus or Solanecio biafrae respectively. Water (or sugar water) and feed intake of each group were measured and recorded daily. Weekly consumption of water and feed was computed for the entire 5 weeks of the experiment. The fasting blood sugar and weight of the test rats were recorded at baseline and weekly. Oral glucose tolerance test and serum insulin were determined at the end of the experiment using blood samples from the test rats. All results were analysed using ANOVA at p[less than or equal to]0.05 and means were separated with the use of Duncan's multiple range tests (SPSS 20.0). The high-fat feed was significantly different from the standard rat feed in the composition of fat (26.79 g) and calories (422.67 kcal). The negative control and the treatment groups got adapted to feeding on the high-calorie diet before the end of the experimental period. Water and feed intakes of the positive control were only significantly higher during the first three and four weeks, respectively. At the end of the experiment, the positive control had the highest weight gain of 22 g which was significantly different at p[less than or equal to]0.05. C. crepidioides and S. biafrae significantly lowered the blood sugar (62.75 and 62.50 mg/dL) of the test rats. A. hybridus prevented insulin resistance by the attainment of peak level at 30 min alongside the positive control. There was a significant increase in the insulin level of the negative control while the vegetables prevented increased production of insulin. Key words: Blood sugar, Diabetes, Feeding behaviour, High-calorie, Insulin, Obesity, Vegetable, Weight gain, INTRODUCTION Eating (feeding) behaviour has considerable influence on health and it is the major risk factor for chronic diseases. People engage in eating behaviour as a matter of survival in [...]

Background Masked hypertension defined as having normal office blood pressure (BP) but hypertension detected by continuous BP monitoring has been observed in children and adolescents with type 1 diabetes (T1D). However, no study has evaluated whether masked hypertension is associated with glycemic variability (GV) in these patients. We hypothesized that masked hypertension might be associated with high GV in patients with T1D. Methods This cross-sectional study performed continuous glucose monitoring (CGM) in parallel with ambulatory blood pressure monitoring (ABPM) in T1D patients aged 6-21 years. Patients who had known hypertension were excluded. CGM data from the same day as ABPM was calculated for GV including standard deviation (SD), coefficient of variation (CV) of glucose levels, and unstable glycemia which was defined as having a CV of glucose levels [greater than or equal to] 36%. Results Thirty-three patients had complete ABPM and CGM data. Mean (SD) age was 13.8 (3.8) years and mean (SD) duration of T1D was 5.4 (3.6) years. All patients had normal office BP, but ABPM showed masked hypertension in 9 patients (27%). In comparison with normotensive patients, patients with masked hypertension had longer duration of T1D (7.4 vs. 4.6 years, p = 0.049), higher insulin requirement (1.2 vs. 0.9 units/kg/day, p = 0.049), and higher SD of glucose (70.3 vs. 47.9 mg/dl, p = 0.038). Masked hypertension group had a greater number of patients (71% vs. 19%, p = 0.02) with unstable glycemia. Multivariate analysis revealed that unstable glycemia was associated with masked hypertension. Conclusions The presence of unstable glycemia in children and adolescents with T1D is associated with masked hypertension., Author(s): Warinpapha Homhuan [sup.1] , Preamrudee Poomthavorn [sup.1] , Witchuri Paksi [sup.1] , Patcharin Khlairit [sup.1] , Arkom Nongnuch [sup.2] , Kwanchai Pirojsakul [sup.1] [sup.3] Author Affiliations: (1) grid.10223.32, 0000 [...]

The etiology of type 1 diabetes has polygenic and environmental determinants that lead to autoimmune responses against pancreatic [beta] cells and promote [beta] cell death. The autoimmunity is considered silent without metabolic consequences until late preclinical stages,and it remains unknown how early in the disease process the pancreatic [beta] cell is compromised. To address this, we investigated preprandial nonfasting and postprandial blood glucose concentrations and islet autoantibody development in 1,050 children with high genetic risk of type 1 diabetes. Pre- and postprandial blood glucose decreased between 4 and 18 months of age and gradually increased until the final measurements at 3.6 years of age. Determinants of blood glucose trajectories in the first year of life included sex, body mass index, glucose-related genetic risk scores, and the type 1 diabetes-susceptible INS gene. Children who developed islet autoantibodies had early elevations in blood glucose concentrations. A sharp and sustained rise in postprandial blood glucose was observed at around 2 months prior to autoantibody seroconversion, with further increases in postprandial and, subsequently, preprandial values after seroconversion. These findings show heterogeneity in blood glucose control in infancy and early childhood and suggest that islet autoimmunity is concurrent or subsequent to insults on the pancreatic islets., Introduction The supply, uptake, and metabolism of glucose are cornerstones of energy production for cell and organ function and survival. Blood glucose levels are regulated by a multitude of hormones [...]

Glucose control and weight loss are cornerstones of type 2 diabetes treatment. Currently, only glucagon-like peptide-1 (GLP1) analogs are able to achieve both weight loss and glucose tolerance. Both glucose and body weight are regulated by the brain, which contains GLP1 receptors (GLP1R). Even though the brain is poised to mediate the effects of GLP1 analogs, it remains unclear whether the glucose- and body weight-lowering effects of long-acting GLP1R agonists are via direct action on CNS GLP1R or the result of downstream activation of afferent neuronal GLP1R We generated mice with either neuronal or visceral nerve-specific deletion of Glp1r and then administered liraglutide, a long-acting GLP1R agonist. We found that neither reduction of GLP1R in the CNS nor in the visceral nerves resulted in alterations in body weight or food intake in animals fed normal chow or a high-fat diet. Liraglutide treatment provided beneficial glucose-lowering effects in both chow- and high-fat-fed mice lacking GLP1R in the CNS or visceral nerves; however, liraglutide was ineffective at altering food intake, body weight, or causing a conditioned taste aversion in mice lacking neuronal GLP1R These data indicate that neuronal GLP1Rs mediate body weight and anorectic effects of liraglutide, but are not required for glucose-lowering effects., Introduction Glucagon-like peptide-1 (GLP1) is a peptide produced both by intestinal enteroendocrine cells and a discrete population of hindbrain neurons. GLP1 acts through a G-protein-coupled receptor (GLP1R) expressed on pancreatic [...]

Objective: Intensive insulin therapy reduces mortality in subgroups of intensive care unit (ICU) patients, and awareness of the importance of blood glucose level (BGL) control has increased among ICU physicians and nurses. The impact of insulin treatment strategies on mortality may be influenced by their efficacy in achieving the target BGL range. We assessed the efficacy of an insulin treatment strategy in maintaining BGL within the target range, and we compared ICU mortality in patients who did and did not reach the BGL target. Design: Prospective cohort study. Setting: 12-bed medical ICU in a tertiary teaching hospital. Patients and participants: Adults consecutively admitted over a 9-month period to an ICU where standard care included an insulin treatment strategy aimed at maintaining BGL ≤ 7 mmol/l. Measurements and main results: 105 patients were included. Median SAPS II was 45 (31-54). Failure to control BGL (mean capillary BGL > 7 mmol/l after initial hyperglycemia correction) occurred in 32 patients (31.1%) and was associated with a significant increase in ICU mortality (56.2 vs. 23.3% in patients with successful BGL control). In the multivariate analysis, failure to control BGL independently predicted death in the ICU (OR 5.9, 2.1-16.6, p < 0.001). Conclusions: Failure to control BGL despite intensive insulin therapy was common and independently associated with ICU mortality. Failure to control BGL may considerably affect the overall impact of insulin treatment strategies on mortality. Keywords Hyperglycemia * Insulin * Intensive care unit * Mortality * Critical illness * Treatment failure, Introduction Hyperglycemia is associated with increased mortality in patients with specific conditions such as acute myocardial infarction [1], stroke [2, 3], or trauma [4]. In critically ill patients, hyperglycemia is [...]

Byline: Subhash. Todi, Mahuya. Bhattacharya Background: Acute hyperglycemia, hypoglycemia and glycemic variability (GV) have been found to be the three principal domains of glycemic control, which can adversely affect patient [...]

Chromium is an essential trace mineral. Trivalent chromium acts as a cofactor for insulin and is therefore an integral part of the cellular response to this hormone. Chromium deficiency has [...]