scholarly journals Lumacaftor/ivacaftor therapy fails to increase insulin secretion in F508del/F508del CF patients

2020 ◽  
Author(s):  
Amir Moheet ◽  
Daniel Beisang ◽  
Lin Zhang ◽  
Scott D. Sagel ◽  
Jill M. VanDalfsen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Increase Insulin Secretion

Insulin increases thermogenesis in rat skeletal muscle following exercise

1985 ◽  
Vol 248 (1) ◽  
pp. E148-E151
Author(s):  
T. W. Balon ◽  
A. Zorzano ◽  
M. N. Goodman ◽  
N. B. Ruderman
Keyword(s):  
Skeletal Muscle ◽  
Insulin Secretion ◽  
Glycogen Synthesis ◽  
O2 Consumption ◽  
Rat Skeletal Muscle ◽  
Additional Energy ◽  
Rat Muscle ◽  
Prior Exercise ◽  
Increase Insulin Secretion ◽  
Stimulation Of

Insulin increased O2 consumption in isolated perfused rat muscle for upward of 2 h after a treadmill run. Insulin did not increase O2 consumption in nonexercised rats, nor did prior exercise increase O2 consumption in the absence of added insulin. The stimulation of glycogen synthesis by insulin was also enhanced in muscle of previously exercised rats. The additional energy required for this was not sufficient to account for the increase in O2 consumption, however. The results indicate that insulin increases thermogenesis in skeletal muscle after exercise. They also raise the possibility that in intact organisms the thermogenic effect of foods that increase insulin secretion could be increased by prior exercise.

scholarly journals Insulin secretory effect of sitagliptin: assessment with a hyperglycemic clamp combined with a meal challenge

2018 ◽  
Vol 314 (4) ◽  
pp. E406-E412
Author(s):  
Sudha S. Shankar ◽  
R. Ravi Shankar ◽  
Lori A. Mixson ◽  
Deborah L. Miller ◽  
Helmut O. Steinberg ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Direct Action ◽  
Intraclass Correlation ◽  
Significant Treatment ◽  
Postprandial Glycemia ◽  
Hyperglycemic Clamp ◽  
The Face ◽  
Increase Insulin Secretion ◽  
Meal Challenge

Sitagliptin, a dipeptidyl peptidase-IV inhibitor (DPP-4), sustains activity of the incretin hormones GLP-1 and GIP and improves hyperglycemia in Type 2 diabetes mellitus (T2DM). It has however proven challenging to quantify the effect of sitagliptin on rates of insulin secretion (ISR) during a prandial challenge. The tight feedback governance of ISR by plasma glucose means that in the face of treatment-related lowering of postprandial glycemia, corresponding stimulation of ISR is lessened. We postulated that sustaining a stable level of moderate hyperglycemia before and during a meal challenge (MC) would be a platform that enables greater clarity to assess the effect of sitagliptin on ISR and an approach that could be valuable to evaluate novel targets that increase insulin secretion directly and by augmenting incretins. A hyperglycemic clamp (HGC) at 160 mg/dl was conducted in 12 healthy volunteers (without diabetes) for 6 h; 3 h into the HGC, MC was administered while maintaining stable hyperglycemia of the HGC for an additional 3 h. Modeling of C-peptide response was used to calculate ISR. In crossover design of three periods (sitagliptin twice and placebo once), the effect of sitagliptin vs. placebo on ISR and the reproducibility of the response to sitagliptin were assessed. Sitagliptin increased ISR compared with placebo by 50% and 20% during the HGC alone and the HGC-MC phases, respectively ( P < 0.001 for both). There was an associated significant treatment-based increase in circulating insulin, as well as active levels of GLP-1. Robust reproducibility of the sitagliptin-mediated ISR response was observed; the intraclass correlation value was 0.94. The findings delineate the effect of sitagliptin to stimulate insulin secretion, and these benchmark data also demonstrate that an HGC-MC can be a useful platform for interrogating therapeutic targets that could potentially modulate ISR via direct action on beta-cells as well as by augmenting release or action of incretins.

Soybean- and olive-oils-enriched diets increase insulin secretion to glucose stimulus in isolated pancreatic rat islets

1998 ◽  
Vol 65 (2) ◽  
pp. 289-294 ◽  
Author(s):  
MariaC Picinato ◽  
Rui Curi ◽  
UbiratanF Machado ◽  
AngeloR Carpinelli
Keyword(s):  
Insulin Secretion ◽  
Rat Islets ◽  
Olive Oils ◽  
Increase Insulin Secretion

scholarly journals Adipose differentiation-related protein regulates lipids and insulin in pancreatic islets

2010 ◽  
Vol 299 (2) ◽  
pp. E249-E257 ◽  
Author(s):  
D. M. Faleck ◽  
K. Ali ◽  
R. Roat ◽  
M. J. Graham ◽  
R. M. Crooke ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Acid Uptake ◽  
Mrna Levels ◽  
Related Protein ◽  
Β Cells ◽  
Adipose Differentiation ◽  
Increase Insulin Secretion

The excess accumulation of lipids in islets is thought to contribute to the development of diabetes in obesity by impairing β-cell function. However, lipids also serve a nutrient function in islets, and fatty acids acutely increase insulin secretion. A better understanding of lipid metabolism in islets will shed light on complex effects of lipids on β-cells. Adipose differentiation-related protein (ADFP) is localized on the surface of lipid droplets in a wide range of cells and plays an important role in intracellular lipid metabolism. We found that ADFP was highly expressed in murine β-cells. Moreover, islet ADFP was increased in mice on a high-fat diet (3.5-fold of control) and after fasting (2.5-fold of control), revealing dynamic changes in ADFP in response to metabolic cues. ADFP expression was also increased by addition of fatty acids in human islets. The downregulation of ADFP in MIN6 cells by antisense oligonucleotide (ASO) suppressed the accumulation of triglycerides upon fatty acid loading (56% of control) along with a reduction in the mRNA levels of lipogenic genes such as diacylglycerol O-acyltransferase-2 and fatty acid synthase. Fatty acid uptake, oxidation, and lipolysis were also reduced by downregulation of ADFP. Moreover, the reduction of ADFP impaired the ability of palmitate to increase insulin secretion. These findings demonstrate that ADFP is important in regulation of lipid metabolism and insulin secretion in β-cells.

scholarly journals Alpha-to-beta cell trans-differentiation for treatment of diabetes

2021 ◽  
Author(s):  
Mohamed Saleh ◽  
George K. Gittes ◽  
Krishna Prasadan
Keyword(s):  
United States ◽  
Insulin Secretion ◽  
Financial Burden ◽  
Cell Mass ◽  
The United States ◽  
Radical Cure ◽  
Β Cell ◽  
Treatment Of Diabetes ◽  
Increase Insulin Secretion ◽  
Potential Strategy

Diabetes mellitus is a significant cause of morbidity and mortality in the United States and worldwide. According to the CDC, in 2017, ∼34.2 million of the American population had diabetes. Also, in 2017, diabetes was the seventh leading cause of death and has become the number one biomedical financial burden in the United States. Insulin replacement therapy and medications that increase insulin secretion and improve insulin sensitivity are the main therapies used to treat diabetes. Unfortunately, there is currently no radical cure for the different types of diabetes. Loss of β cell mass is the end result that leads to both type 1 and type 2 diabetes. In the past decade, there has been an increased effort to develop therapeutic strategies to replace the lost β cell mass and restore insulin secretion. α cells have recently become an attractive target for replacing the lost β cell mass, which could eventually be a potential strategy to cure diabetes. This review highlights the advantages of using α cells as a source for generating new β cells, the various investigative approaches to convert α cells into insulin-producing cells, and the future prospects and problems of this promising diabetes therapeutic strategy.

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