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Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion
It is demonstrated that SGLT2 is expressed in glucagon-secreting alpha cells of the pancreatic islets, and dapagliflozin treatment further promotes glucagon secretion and hepatic gluconeogenesis in healthy mice, thereby limiting the decrease of plasma glucose induced by fasting. Expand
L-leucine and a nonmetabolized analogue activate pancreatic islet glutamate dehydrogenase
Data is presented consistent with the idea that BCH induces insulin release through the allosteric activation of glutamate dehydrogenase, which is compatible with the fuel hypothesis, which states that the secretory response to nutrient secretagogues depends always on an increase of catabolic fluxes in the islet cells. Expand
The lipid phosphatase SHIP2 controls insulin sensitivity
The results show that SHIP2 is a potent negative regulator of insulin signalling and insulin sensitivity in vivo. Expand
n-3 fatty acids and the metabolic syndrome.
The use of n-3 PUFAs should be considered in more global strategies including changes in lifestyle, such as adhering to a healthy Mediterranean type of diet and practicing regular physical exercise. Expand
Changes in Glucagon-like Peptide-1 (GLP-1) Secretion after Biliopancreatic Diversion or Vertical Banded Gastroplasty in Obese Subjects
Findings support the postulated role of GLP-1, secreted by the hindgut, as a key mediator of the antidiabetic effects of bariatric operations. Expand
Pancreatic Beta-Cell Web: Its Possible Role in Insulin Secretion
A cortical band of fine microfilaments is consistently observed in the beta cells of the rat pancreas. Alteration of this cell web by cytochalasin B is associated with an enhancement ofExpand
Meal frequency and timing in health and disease
Emerging findings from studies of animal models and human subjects suggest that intermittent energy restriction periods of as little as 16 h can improve health indicators and counteract disease processes. Expand
Alloxan toxicity to the pancreatic B-cell. A new hypothesis.
  • W. Malaisse
  • Chemistry, Medicine
  • Biochemical pharmacology
  • 15 November 1982
Stimulation of pancreatic islet metabolism and insulin release by a nonmetabolizable amino acid.
The activation of glutamate dehydrogenase by BCH may account for the insulin-releasing capacity of the leucine analog and be responsible for the dose-related increase in 14CO2 output from islets prelabeled with L-[U-14C]glutamine. Expand
Impaired activity of rat pancreatic islet mitochondrial glycerophosphate dehydrogenase in protein malnutrition.
Findings support the view that an impaired activity of pancreatic B-cell mitochondrial glycerophosphate dehydrogenase contributes, possibly in association with other enzymatic anomalies, to the perturbation of islet function in protein malnutrition. Expand