Abstract
The endocrine pancreas plays a key role in metabolism. Procyanidins (GSPE) targets β-cells and glucagon-like peptide-1 (GLP-1)-producing cells; however, there is no information on the effects of GSPE on glucagon. We performed GSPE preventive treatments administered to Wistar rats before or at the same time as they were fed a cafeteria diet during 12 or 17 weeks. We then measured the pancreatic function and GLP-1 production. We found that glucagonemia remains modified by GSPE pre-treatment several weeks after the treatment has finished. The animals showed a higher GLP-1 response to glucose stimulation, together with a trend towards a higher GLP-1 receptor expression in the pancreas. When the GSPE treatment was administered every second week, the endocrine pancreas behaved differently. We show here that glucagon is a more sensitive parameter than insulin to GSPE treatments, with a secretion that is highly linked to GLP-1 ileal functionality and dependent on the type of treatment.
Highlights
The proper functioning of the endocrine pancreas plays a key role in the whole-body energy homeostasis
Rats that have had a cafeteria diet for 12 weeks have increased glucose and insulin, resulting in increased homeostatic model assessment for insulin resistance (HOMA-IR) and increased HOMA-β compared to the control group (Table 1)
These results are in agreement with previous literature that states that the cafeteria diet causes peripheral insulin resistance, and the pancreas compensates for this by producing more insulin [18]
Summary
The proper functioning of the endocrine pancreas plays a key role in the whole-body energy homeostasis. Studies with glucagon receptor knockout mice (GlcR−/−) together with streptozotocin-induced destruction of the β-cells indicate that hyperglucagonaemia may be far more important than previously recognized [3]. These results highlight the role played by glucagon in diabetes and indicate that chemical modulation of glucagon release may represent a way of achieving improved glycemic control in diabetes. Α-cells retain near normal responsiveness to GLP-1 infusion, since diabetic and nondiabetic subjects showed similar inhibition of glucagon secretion [7]. It Ihtashabseebnesehnowshnotwhant athnaatcuante adcousteeodf gorsaepoesfegedra-dpeersieveedd-dperroicvyeadnipdrinoceyxatnraidctin(GeSxPtEra)ct ca(nGiSnPcEre) acsaen pinlcarsemasaeGpLlaPs-m1a[1G1L]Pa-n1d[1p1]reavnednpt rtehveendtetchreeadseecrineaGseLiPn-G1 LaPss-1ocaisastoecdiawteidthwaith caafectearfeiatedriiaetd[i1e2t][.12F]u. MataetreiarilaslasnadndMMetehtohdosds 2.12..1P.rPoraonatnhtohcoycaynaindiindiEnxEtrxatcrat ct ThTehgergarpaepseeseededexetrxatrcatsctesnernicrhicehdeidnipnrporaonatnhtohcoycaynaidniidnsin(sG(SGPSEP)Ew) ewreerkeinkdinlydlpyrporvoidveidded bybLyeLs eDséDriévréisvRésésRinésiqinuieqsueetsTeetrpTéenrpiqéuneisqu(Desax(,DFarxa,nFcera).nWcee).uWseed ubsaetcdhbnautcmhbneursm1b2e4r,0s2192[41,30]29 1a7n[1-d1w73-e1w]e7aek4ne,cd8ka6c1f0ea7tf4(eec,r8toie6anr0itsaat(uicsnodtuinyndtgaayinn2ad1inn.td6gh%et2h11efl.26a1-%wv2-aewfnela-ek3vec-akoanlfc-ea3mtf-eeoortlienarmoisamtounsedtoruysmd,, rye4er,1ssrp.,e6e4s%cp1t.ei6dvc%tieimlvydee.ilrmys.+ertrsi+mtreimrse)rfso)rfotrhethe
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
