scholarly journals Stress and glucocorticoid inhibit apical GLUT2-trafficking and intestinal glucose absorption in rat small intestine

2004 ◽  
Vol 560 (1) ◽  
pp. 281-290 ◽  
Author(s):  
Emma J. Shepherd ◽  
Philip A. Helliwell ◽  
Oliver J. Mace ◽  
Emma L. Morgan ◽  
Nick Patel ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Absorption ◽  
Rat Small Intestine ◽  
Intestinal Glucose Absorption

scholarly journals Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2474
Author(s):  
Lyudmila V. Gromova ◽  
Serguei O. Fetissov ◽  
Andrey A. Gruzdkov
Keyword(s):  
Small Intestine ◽  
Blood Glucose ◽  
Metabolic Diseases ◽  
Glucose Absorption ◽  
Cellular Mechanisms ◽  
Physiological Conditions ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
New Strategy ◽  
Intestinal Glucose Absorption

The worldwide prevalence of metabolic diseases such as obesity, metabolic syndrome and type 2 diabetes shows an upward trend in recent decades. A characteristic feature of these diseases is hyperglycemia which can be associated with hyperphagia. Absorption of glucose in the small intestine physiologically contributes to the regulation of blood glucose levels, and hence, appears as a putative target for treatment of hyperglycemia. In fact, recent progress in understanding the molecular and cellular mechanisms of glucose absorption in the gut and its reabsorption in the kidney helped to develop a new strategy of diabetes treatment. Changes in blood glucose levels are also involved in regulation of appetite, suggesting that glucose absorption may be relevant to hyperphagia in metabolic diseases. In this review we discuss the mechanisms of glucose absorption in the small intestine in physiological conditions and their alterations in metabolic diseases as well as their relevance to the regulation of appetite. The key role of SGLT1 transporter in intestinal glucose absorption in both physiological conditions and in diabetes was clearly established. We conclude that although inhibition of small intestinal glucose absorption represents a valuable target for the treatment of hyperglycemia, it is not always suitable for the treatment of hyperphagia. In fact, independent regulation of glucose absorption and appetite requires a more complex approach for the treatment of metabolic diseases.

scholarly journals Effect of mazindol on glucose absorption in everted rat small intestine.

1986 ◽  
Vol 87 (6) ◽  
pp. 649-654
Author(s):  
Masahiko TSUCHIYA ◽  
Shuji INOUE ◽  
Masayuki SATTA ◽  
Hideki YOSHIMURA ◽  
Masataka ARITA ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Absorption ◽  
Rat Small Intestine

scholarly journals Multifaceted interplay among mediators and regulators of intestinal glucose absorption: potential impacts on diabetes research and treatment

2015 ◽  
Vol 309 (11) ◽  
pp. E887-E899 ◽  
Author(s):  
Leo Ka Yu Chan ◽  
Po Sing Leung
Keyword(s):  
Small Intestine ◽  
Blood Glucose ◽  
Critical Role ◽  
Glucose Absorption ◽  
Therapeutic Interventions ◽  
Diabetes Research ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Patients With Diabetes ◽  
Intestinal Glucose Absorption

Glucose is the prominent molecule that characterizes diabetes and, like the vast majority of nutrients in our diet, it is absorbed and enters the bloodstream directly through the small intestine; hence, small intestine physiology impacts blood glucose levels directly. Accordingly, intestinal regulatory modulators represent a promising avenue through which diabetic blood glucose levels might be moderated clinically. Despite the critical role of small intestine in blood glucose homeostasis, most physiological diabetes research has focused on other organs, such as the pancreas, kidney, and liver. We contend that an improved understanding of intestinal regulatory mediators may be fundamental for the development of first-line preventive and therapeutic interventions in patients with diabetes and diabetes-related diseases. This review summarizes the major important intestinal regulatory mediators, discusses how they influence intestinal glucose absorption, and suggests possible candidates for future diabetes research and the development of antidiabetic therapeutic agents.

scholarly journals Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2

2007 ◽  
Vol 582 (1) ◽  
pp. 379-392 ◽  
Author(s):  
Oliver J. Mace ◽  
Julie Affleck ◽  
Nick Patel ◽  
George L. Kellett
Keyword(s):  
Small Intestine ◽  
Sweet Taste ◽  
Glucose Absorption ◽  
Taste Receptors ◽  
Rat Small Intestine ◽  
Sweet Taste Receptors

scholarly journals Kinetics and mechanisms of glucose absorption in the rat small intestine under physiological conditions

2012 ◽  
Vol 03 (02) ◽  
pp. 191-200 ◽  
Author(s):  
Andrei A. Gruzdkov ◽  
Liudmila V. Gromova ◽  
Nadezhda M. Grefner ◽  
Yan Yu. Komissarchik
Keyword(s):  
Small Intestine ◽  
Glucose Absorption ◽  
Rat Small Intestine ◽  
Physiological Conditions

Hydrolyzed guar gum decreases postprandial blood glucose and glucose absorption in the rat small intestine

2009 ◽  
Vol 29 (6) ◽  
pp. 419-425 ◽  
Author(s):  
Toru Takahashi ◽  
Takeo Yokawa ◽  
Noriyuki Ishihara ◽  
Tsutomu Okubo ◽  
Djong-Chi Chu ◽  
...  
Keyword(s):  
Small Intestine ◽  
Blood Glucose ◽  
Guar Gum ◽  
Glucose Absorption ◽  
Postprandial Blood Glucose ◽  
Rat Small Intestine

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.

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