scholarly journals Impaired stimulation of intestinal glucose absorption via hepatoenteral nerves in streptozotocin-diabetic rats

1999 ◽  
Vol 277 (2) ◽  
pp. G285-G291
Author(s):  
Frank Stümpel ◽  
Tomas Kucera ◽  
Kurt Jungermann
Keyword(s):  
Portal Vein ◽  
Insulin Action ◽  
Liver Perfusion ◽  
Late Complication ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
Ex Situ ◽  
Streptozotocin Diabetic Rats ◽  
Intestinal Glucose Absorption ◽  
Absorptive Enterocytes

In an ex situ organ perfusion system, that of the isolated nonrecirculating joint perfusion of rat small intestine and liver, insulin infused into the portal vein increased intestinal glucose absorption. This insulin action against the bloodstream can be blocked by TTX, indicating a propagation of the insulin signal via hepatoenteral nerves, which conforms with previous studies with atropine and carbachol. Insulin action could also be mimicked by dibutyryl cAMP (DBcAMP) acting directly on the absorptive enterocytes. Because autonomic neuropathy is a common late complication of diabetes mellitus, the possible impairment of these nerves in the diabetic state was studied in streptozotocin-diabetic rats. In the isolated joint intestine-liver perfusion, glucose was applied as a bolus into the lumen; its absorption was measured in the portal vein. In 5-day diabetic as well as in control rats, portal insulin, arterial carbachol, and arterial DBcAMP increased intestinal glucose absorption. In 3-mo diabetic rats portal insulin and arterial carbachol failed to stimulate glucose absorption, whereas arterial DBcAMP still did so, indicating an undisturbed function of the absorptive enterocytes. The lack of an effect of portal insulin and arterial carbachol and the unchanged action of DBcAMP in the chronically diabetic rats indicated that the signaling chain via the hepatoenteral nerves was impaired, which is in line with a diabetic neuropathy.

Effect of benfluorex on insulin secretion and insulin action in streptozotocin-diabetic rats

1993 ◽  
Vol 9 (S1) ◽  
pp. 57S-63S ◽  
Author(s):  
Bernard Portha ◽  
Patricia Serradas ◽  
Danielle Bailbé ◽  
Olivier Blondel ◽  
Françoise Picarel
Keyword(s):  
Insulin Secretion ◽  
Insulin Action ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

scholarly journals Sorbitol increases muscle glucose uptake ex vivo and inhibits intestinal glucose absorption ex vivo and in normal and type 2 diabetic rats

2017 ◽  
Vol 42 (4) ◽  
pp. 377-383 ◽  
Author(s):  
Chika Ifeanyi Chukwuma ◽  
Md. Shahidul Islam
Keyword(s):  
Glycemic Control ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
Dependent Manner ◽  
Intestinal Glucose Absorption ◽  
Type 2 Diabetic ◽  
Isolated Rat

Previous studies have suggested that sorbitol, a known polyol sweetener, possesses glycemic control potentials. However, the effect of sorbitol on intestinal glucose absorption and muscle glucose uptake still remains elusive. The present study investigated the effects of sorbitol on intestinal glucose absorption and muscle glucose uptake as possible anti-hyperglycemic or glycemic control potentials using ex vivo and in vivo experimental models. Sorbitol (2.5% to 20%) inhibited glucose absorption in isolated rat jejuna (IC50= 14.6% ± 4.6%) and increased glucose uptake in isolated rat psoas muscle with (GU50= 3.5% ± 1.6%) or without insulin (GU50= 7.0% ± 0.5%) in a concentration-dependent manner. Furthermore, sorbitol significantly delayed gastric emptying, accelerated digesta transit, inhibited intestinal glucose absorption, and reduced blood glucose increase in both normoglycemic and type 2 diabetic rats after 1 h of coingestion with glucose. Data of this study suggest that sorbitol exhibited anti-hyperglycemic potentials, possibly via increasing muscle glucose uptake ex vivo and reducing intestinal glucose absorption in normal and type 2 diabetic rats. Hence, sorbitol may be further investigated as a possible anti-hyperglycemic sweetener.

Oral salmon calcitonin enhances insulin action and glucose metabolism in diet-induced obese streptozotocin-diabetic rats

2014 ◽  
Vol 737 ◽  
pp. 91-96 ◽  
Author(s):  
Michael Feigh ◽  
Sara T. Hjuler ◽  
Kim V. Andreassen ◽  
Sofie Gydesen ◽  
Ida Ottosen ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Salmon Calcitonin ◽  
Insulin Action ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

D-mannitol modulates glucose uptake ex vivo; suppresses intestinal glucose absorption in normal and type 2 diabetic rats

2019 ◽  
Vol 29 ◽  
pp. 30-36 ◽  
Author(s):  
Chika Ifeanyi Chukwuma ◽  
Motlalepula Gilbert Matsabisa ◽  
Ochuko L. Erukainure ◽  
Collins U. Ibeji ◽  
Md. Shahidul Islam
Keyword(s):  
Glucose Uptake ◽  
Ex Vivo ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
Intestinal Glucose Absorption ◽  
Type 2 Diabetic

Effect of Insulin on Intestinal Glucose Absorption in Alloxan Diabetic Rats

Nature ◽  
1948 ◽  
Vol 161 (4102) ◽  
pp. 932-933 ◽  
Author(s):  
A. SOLS ◽  
S. VIDAL ◽  
J. LARBALDE
Keyword(s):  
Glucose Absorption ◽  
Diabetic Rats ◽  
Intestinal Glucose Absorption

scholarly journals Importance of Hepatic Portal Circulation for Insulin Action in Streptozotocin-Diabetic Rats Transplanted with Fetal Pancreases

1979 ◽  
Vol 64 (6) ◽  
pp. 1688-1694 ◽  
Author(s):  
Josiah Brown ◽  
Yoko Mullen ◽  
William R. Clark ◽  
I. Gabriella Molnar ◽  
Diane Heininger
Keyword(s):  
Insulin Action ◽  
Diabetic Rats ◽  
Portal Circulation ◽  
Streptozotocin Diabetic Rats ◽  
Hepatic Portal

d-Fenfluramine improves hepatic insulin action in streptozotocin-diabetic rats

1994 ◽  
Vol 264 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Françoise Picarel-Blanchot ◽  
Danielle Bailbé ◽  
Bernard Portha
Keyword(s):  
Insulin Action ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

scholarly journals Increases in intestinal glucose absorption and hepatic glucose uptake elicited by luminal but not vascular glutamine in the jointly perfused small intestine and liver of the rat

1992 ◽  
Vol 283 (3) ◽  
pp. 759-765 ◽  
Author(s):  
A Gardemann ◽  
Y Watanabe ◽  
V Große ◽  
S Hesse ◽  
K Jungermann
Keyword(s):  
Small Intestine ◽  
Portal Vein ◽  
Superior Mesenteric Artery ◽  
Glucose Uptake ◽  
Mesenteric Artery ◽  
Hepatic Uptake ◽  
Glucose Absorption ◽  
Hepatic Glucose ◽  
Intestinal Glucose Absorption ◽  
Hepatic Glucose Uptake

1. Previous studies have shown that an arterial-to-portal glucose concentration gradient may be an important signal for insulin-dependent net hepatic glucose uptake. It is not known whether intestinal factors also contribute to the regulation of hepatic glucose utilization. This problem was studied in a newly developed model which allows luminal perfusion of the small intestine via the pyloric sphincter and a combined vascular perfusion of the small intestine via the gastroduodenal artery and superior mesenteric artery, and of the liver via the hepatic artery and portal vein. 2. In both the presence and the absence of 1 mM-glutamine in the vascular perfusate, only about 7% of a luminal bolus of 5500 mumol (1 g) of glucose was absorbed by the small intestine, and nothing was taken up by the liver. 3. With small doses of 75-380 mumol (11-55 mg) of luminal glutamine, but not with 300 mumol of alanine, the intestinal absorption of the luminal glucose bolus was increased almost linearly from 7% to a maximum of 40% and the hepatic uptake from 0% to a maximum of 22%. 4. The increase of hepatic glucose uptake caused by luminal glutamine was only observed when the glucose load was applied into the intestinal lumen, rather than into the superior mesenteric artery. 5. The relative hepatic glucose uptake (uptake/portal supply) was enhanced from 0% to 55% with an increase in portal supply by luminal glutamine, whereas with a similar range of portal glucose supply the relative hepatic uptake by the isolated liver, perfused simultaneously via the hepatic artery and portal vein, was slightly decreased, from 20% to 15%. 6. Addition of various amounts of portal glutamine and/or alterations in the Na+ content of the portal perfusate failed to mimic the luminal glutamine-dependent activation of hepatic glucose uptake. Therefore the luminal-glutamine-elicited activation of hepatic glucose uptake was apparently not caused by a simple increase in the portal-arterial glucose gradient, by glutamine itself or by Na(+)-dependent alterations in hepatic cell volume. The results suggest that luminal glutamine caused not only an increase in intestinal glucose absorption by unknown mechanisms but also the generation of one or more humoral or nervous ‘hepatotropic’ signals in the small intestine which enhanced the hepatic uptake of absorbed glucose.

scholarly journals Portal milieu and the interplay of multiple antidiabetic effects after gastric bypass surgery

2019 ◽  
Vol 316 (5) ◽  
pp. G668-G678 ◽  
Author(s):  
Atanu Pal ◽  
David B. Rhoads ◽  
Ali Tavakkoli
Keyword(s):  
Gastric Bypass ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
Rat Strains ◽  
Hepatic Glucose ◽  
Intestinal Glucose Absorption ◽  
Zdf Rats ◽  
Fresh Insight

Diabetes is a worldwide health problem. Roux-en-Y gastric bypass (RYGB) leads to rapid resolution of type 2 diabetes (T2D). Decreased hepatic insulin resistance is key, but underlying mechanisms are poorly understood. We hypothesized that changes in intestinal function and subsequent changes in portal venous milieu drive some of these postoperative benefits. We therefore aimed to evaluate postoperative changes in portal milieu. Two rat strains, healthy [Sprague-Dawley (SD)] and obese diabetic [Zucker diabetic fatty (ZDF)] rats, underwent RYGB or control surgery. After 4 wk, portal and systemic blood was sampled before and during an intestinal glucose bolus to investigate changes in intestinal glucose absorption (Gabsorp) and utilization (Gutil), and intestinal secretion of incretins and glucagon-like peptide-2 (GLP-2). Hepatic activity of dipeptidyl peptidase-4 (DPP4), which degrades incretins, was also measured. RYGB decreased Gabsorp in both rat strains. Gutil increased in SD rats and decreased in ZDF rats. In both strains, there was increased expression of intestinal hexokinase and gluconeogenesis enzymes. Systemic incretin and GLP-2 levels also increased after RYGB. This occurred without an increase in secretion. Hepatic DPP4 activity and expression were unchanged. RYGB perturbs multiple intestinal pathways, leading to decreased intestinal glucose absorption and increased incretin levels in both healthy and diabetic animals. In diabetic rats, intestinal glucose balance shifts toward glucose release. The portal vein as the gut-liver axis may integrate these intestinal changes to contribute to rapid changes in hepatic glucose and hormone handling. This fresh insight into the surgical physiology of RYGB raises the hope of less invasive alternatives. NEW & NOTEWORTHY Portal milieu after gastric bypass surgery is an underinvestigated area. Roux-en-Y gastric bypass perturbs multiple intestinal pathways, reducing intestinal glucose absorption and increasing incretin levels. In diabetic rats, the intestine becomes a net releaser of glucose, increasing portal glucose levels. The portal vein as the gut-liver axis may integrate these intestinal changes to contribute to changes in hepatic glucose handling. This fresh insight raises the hope of less invasive alternatives.

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