Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40

Nature ◽  
2003 ◽  
Vol 422 (6928) ◽  
pp. 173-176 ◽  
Author(s):  
Yasuaki Itoh ◽  
Yuji Kawamata ◽  
Masataka Harada ◽  
Makoto Kobayashi ◽  
Ryo Fujii ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Β Cells ◽  
Pancreatic Β Cells

Free fatty acids stimulate autophagy in pancreatic β-cells via JNK pathway

2010 ◽  
Vol 401 (4) ◽  
pp. 561-567 ◽  
Author(s):  
Koji Komiya ◽  
Toyoyoshi Uchida ◽  
Takashi Ueno ◽  
Masato Koike ◽  
Hiroko Abe ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Jnk Pathway

n-3 polyunsaturated fatty acids and insulin secretion

2014 ◽  
Vol 224 (3) ◽  
pp. R97-R106 ◽  
Author(s):  
Xiaofeng Wang ◽  
Catherine B Chan
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Polyunsaturated Fatty Acids ◽  
Beneficial Effect ◽  
Health Benefits ◽  
Β Cells ◽  
Pancreatic Β Cells

n-3 polyunsaturated fatty acids (PUFAs) are a subgroup of fatty acids with broad health benefits, such as lowering blood triglycerides and decreasing the risk of some types of cancer. A beneficial effect of n-3 PUFAs in diabetes is indicated by results from some studies. Defective insulin secretion is a fundamental pathophysiological change in both types 1 and 2 diabetes. Emerging studies have provided evidence of a connection between n-3 PUFAs and improved insulin secretion from pancreatic β-cells. This review summarizes the recent findings in this regard and discusses the potential mechanisms by which n-3 PUFAs influence insulin secretion from pancreatic β-cells.

scholarly journals Endogenous Fatty Acids Are Essential Signaling Factors of Pancreatic β-Cells and Insulin Secretion

Diabetes ◽  
2018 ◽  
Vol 67 (10) ◽  
pp. 1986-1998 ◽  
Author(s):  
Sebastian Hauke ◽  
Kaya Keutler ◽  
Prasad Phapale ◽  
Dmytro A. Yushchenko ◽  
Carsten Schultz
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals Mitochondrial Functional State in Clonal Pancreatic β-Cells Exposed to Free Fatty Acids

2003 ◽  
Vol 278 (22) ◽  
pp. 19709-19715 ◽  
Author(s):  
Vasilij Koshkin ◽  
Xiaolin Wang ◽  
Philipp E. Scherer ◽  
Catherine B. Chan ◽  
Michael B. Wheeler
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Functional State ◽  
Β Cells ◽  
Pancreatic Β Cells

Congenital hyperinsulinism due to compound heterozygous mutations in ABCC8 responsive to diazoxide therapy

2020 ◽  
Vol 33 (5) ◽  
pp. 671-674
Author(s):  
Tashunka Taylor-Miller ◽  
Jayne Houghton ◽  
Paul Munyard ◽  
Yadlapalli Kumar ◽  
Clinda Puvirajasinghe ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Compound Heterozygous ◽  
Congenital Hyperinsulinism ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Newborn Period ◽  
Case Presentation ◽  
Male Baby ◽  
Common Causes ◽  
Compound Heterozygous Mutations

AbstractBackgroundCongenital hyperinsulinism (CHI), a condition characterized by dysregulation of insulin secretion from the pancreatic β cells, remains one of the most common causes of hyperinsulinemic, hypoketotic hypoglycemia in the newborn period. Mutations in ABCC8 and KCNJ11 constitute the majority of genetic forms of CHI.Case presentationA term macrosomic male baby, birth weight 4.81 kg, born to non-consanguineous parents, presented on day 1 of life with severe and persistent hypoglycemia. The biochemical investigations confirmed a diagnosis of CHI. Diazoxide was started and progressively increased to 15 mg/kg/day to maintain normoglycemia. Sequence analysis identified compound heterozygous mutations in ABCC8 c.4076C>T and c.4119+1G>A inherited from the unaffected father and mother, respectively. The mutations are reported pathogenic. The patient is currently 7 months old with a sustained response to diazoxide.ConclusionsBiallelic ABCC8 mutations are known to result in severe, diffuse, diazoxide-unresponsive hypoglycemia. We report a rare patient with CHI due to compound heterozygous mutations in ABCC8 responsive to diazoxide.

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