Acylated ghrelin, GLP-17-36 and insulin were not different between trials (P>004)
Post-breakfast area under the curve (AUC) for NEFA (P<05) and GIP1-42 (P<01) were greater during ER compared with EB. Fat oxidation was greater (P<01) and carbohydrate oxidation was lower (P<01) during ER, but energy expenditure was not different between trials (P=058).CONCLUSIONS: These results suggest that 24 h severe ER does not affect appetite regulation or energy intake in the subsequent 48 h. This style of dieting may be conducive to maintenance of a negative EB by limiting compensatory eating behaviour, and therefore may assist with weight loss.Incretin based therapies: bone protective effects.American University of Beirut-Medical Center, 3 Dag Hammarskjold Plaza, 8th Type 2 Diabetes Mellitus (T2D) and osteoporosis have been found recently to be tightly correlated.
In fact, T2D can result in bone loss through different mechanisms resulting in alteration of bone matrix and inhibition of bone formation. API Hormones and Regulation increases significantly. New antidiabetic agents, dipeptidyl peptidase-4 inhibitors and glucagon like peptide -1 agonists have shown promise in many fields beyond glycemic control. Benefits on the skeletal system are multiple through direct stimulation of osteoblasts, inhibition of advanced glycation end products and inhibition of bone resorption. However, API Hormones and Regulation in humans is still not enough to allow definitive conclusions.Interaction between Munc13-1 and RIM is critical for glucagon-like peptide-1 mediated rescue of exocytotic defects in Munc13-1 deficient pancreatic OBJECTIVE: Glucagon-like peptide-1 (GLP-1) rescues insulin secretory deficiency in type 2 diabetes partly via cAMP actions on exchange protein directly activated by cAMP (Epac2) and protein kinase A (PKA)-activated Rab3A-interacting molecule 2 (Rim2). We had reported that haplodeficient Munc13-1(+/-) mouse islet beta-cells exhibited reduced insulin secretion, causing glucose intolerance.
Munc13-1 binds Epac2 and Rim2, but their functional interactions remain unclear.RESEARCH DESIGN AND METHODS: We used Munc13-1(+/-) islet beta-cells to examine the functional interactions between Munc13-1 and Epac2 and PKA. GLP-1 stimulation of Munc13-1(+/-) islets normalized the reduced biphasic insulin secretion by its actions on intact islet cAMP production and normal Epac2 and RESULTS: To determine which exocytotic steps caused by Munc13-1 deficiency are rescued by Epac2 and PKA, we used patch-clamp capacitance measurements, showing that 1) cAMP restored the reduced readily releasable pool (RRP) and partially restored refilling of a releasable pool of vesicles in Munc13-1(+/-) beta-cells, [8-(4-chloro-phenylthio)-2'-O-methyladenosine-3',5'-cyclic monophosphate] partially restored the reduced RRP and refilling of a releasable pool of vesicles, and 3) PKA blockade by H89 (leaving Epac intact) impaired cAMP ability to restore the RRP and refilling of a releasable pool of vesicles. Conversely, partially restored refilling of a releasable pool of vesicles. To determine specific contributions within Epac-Rim2-Munc13-1 interaction sites accounting for cAMP rescue of exocytosis caused by Munc13-1 deficiency, we found that blockade of Rim2-Munc13-1 interaction with Rim-Munc13-1-binding domain peptide abolished cAMP rescue, whereas blockade of Epac-Rim2 interaction with Rim2-PDZ peptide only moderately reduced refilling with little effect on RRP.CONCLUSIONS: cAMP rescue of priming defects caused by Munc13-1 deficiency via Epac and PKA signaling pathways requires downstream Munc13-1-Rim2 interaction.Gastrointestinal motility, gut hormone secretion, and energy intake after oral loads of free fatty acid or triglyceride in older and middle-aged men.
Imaging and Research, Hvidovre Hospital, Kettegård Allé 30, DK-2650 Hvidovre, Imaging and Research, Hvidovre Hospital, Kettegård Allé 30, DK-2650 Hvidovre, Hvidovre, Denmark; Novo Nordisk Foundation Centre for Basic Metabolic Research, University of Copenhagen, Blegdamsvej 3A, DK-2200 Copenhagen, Denmark.Copenhagen, Blegdamsvej 3A, DK-2200 Copenhagen, Denmark; Department of Biomedical Sciences, University of Copenhagen, Blegdamsvej 3A, DK-2200 In young individuals, oral free fatty acid delays gastric emptying, promotes gut hormone release, and reduces energy intake more than an isocaloric load of triglyceride does. The objective of this study was to compare the effects of the free fatty acid oleic acid (OA) and the triglyceride olive oil (OO) on gastrointestinal motility, gut hormone secretion, and energy intake in older and middle-aged healthy volunteers. In a double-blind, randomized, cross-over, study 10 older (age 83 ± 3 (mean ± SD) years) and 10 middle-aged (age 43 ± 8 years) men were examined on two occasions to evaluate the effect of isocaloric and isovolaemic loads of radiolabelled OA or OO on gastric emptying, oro-caecal transit, glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) secretions, and energy intake. Gastric emptying was slower in older than in middle-aged men (lipid p < 001, water p = 010), while no difference between these groups was found for oro-caecal transit. In comparison with OO, OA caused slower gastric emptying (lipid p < 001, water p = 020) and faster oro-caecal transit (p = 025).