Glucose tolerance test

Summary

The glucose tolerance test (GTT, not to be confused with GGT test) is a medical test in which glucose is given and blood samples taken afterward to determine how quickly it is cleared from the blood. The test is usually used to test for diabetes, insulin resistance, impaired beta cell function, and sometimes reactive hypoglycemia and acromegaly, or rarer disorders of carbohydrate metabolism. In the most commonly performed version of the test, an oral glucose tolerance test (OGTT), a standard dose of glucose is ingested by mouth and blood levels are checked two hours later. Many variations of the GTT have been devised over the years for various purposes, with different standard doses of glucose, different routes of administration, different intervals and durations of sampling, and various substances measured in addition to blood glucose. History The glucose tolerance test was first described in 1923 by Jerome W. Conn. The test was based on the previous work in 1913 by A. T.

Official source

https://en.wikipedia.org/wiki/Glucose_tolerance_test

About this result

This page is automatically generated and may contain information that is not correct, complete, up-to-date, or relevant to your search query. The same applies to every other page on this website. Please make sure to verify the information with EPFL's official sources.

Related publications (23)

Related publications

Related people (4)

, , ,

Related people

Related units (4)

Related units

Related concepts (12)

Related concepts

Related courses (1)

Related courses

Related lectures (1)

Related lectures

Pancreatic beta cells play a major role in the regulation of glucose homeostasis by secreting insulin in response to elevated blood glucose levels. A gradual deterioration of functional beta cell mass and the chronic elevation of blood glucose levels are central to development of type 2 diabetes. While the etiologies of Type 2 diabetes and age-related metabolic complications are complex, they are often associated with a decline of intracellular nicotinamide adenine dinucleotide (NAD+). NAD+ levels are maintained through the balance between its synthesis from NAD+ precursors and its degradation by several families of enzymes, including the sirtuin family of protein deacetylases, the ADP-ribosyl transferase enzymes (ARTDs or PARPs) and cADP ribose hydrolases (CD38). NAD+ declines are mostly associated with increased NAD+ consumption, which can be counteracted by dietary supplementation of NAD+ precursors. However, our knowledge on how different tissues utilize and respond to different NAD+ precursors for NAD+ synthesis is still incomplete. This, in turn, limits our ability to provide therapeutic benefits in clinical settings. In this project, we aim to understand the relevance of a particular NAD+ precursor, nicotinamide riboside (NR), in beta cell physiology and its potential use to treat beta cell dysfunction. To do so, we have used mice that are deficient for nicotinamide riboside kinase 1 (NRK1), the first and rate-limiting enzyme for the transformation of NR into NAD+. We demonstrate that NRK1 whole body knockout mice exhibit impaired insulin secretion after a meal or upon glucose challenge when fed a high fat diet. However, NRK1 deficiency in beta cell was not the causality for beta cell failure as differences observed in the NRK1 whole body KO mice were not phenocopied in NRK1 beta cell specific KO mice. Aged NRK1 whole body KO mice also exhibited dysfunctional beta cells and significant loss of insulin content and beta cell mass. Furthermore, NRK1 deficiency exacerbates the decline of NAD+ bioavailability and mitochondria function with age, even promoting fibrosis in multiple tissues. Together, our data suggests that endogenous NR metabolism is critical in maintaining whole body NAD+ homeostasis and to protect against mitochondria dysfunction and stress-related cell responses in pancreatic beta cells.

EPFL2022

Genistein increases the thermogenic program of subcutaneous WAT and increases energy expenditure in mice

Lilia Noriega Lopez, Laura Alejandra Velazquez Villegas

White adipose tissue (WAT) can differentiate into beige adipose tissue by the browning process. Some polyphenols, including isoflavones, particularly genistein, are suggested to increase the expression of browning markers. There is evidence that consumption of genistein can attenuate body weight gain and improve glucose tolerance and blood lipid levels. The aim of the present study was to investigate the potential mechanisms of stimulation by which genistein activates the browning of WAT. We studied the stimulation of the expression of browning markers in the following models: mice fed genistein; preadipocytes from 3 T3-L1 cells; and the stromal vascular fraction (SVF) from the inguinal adipose tissue of mice. The results indicated that genistein can stimulate the browning process by at least two mechanisms. An indirect mechanism was involved in the induction of PGC-1 alpha/FNDC5 in skeletal muscle leading to an increase in the myokine irisin. In preadipocytes, irisin was able to increase the expression of Ucpl and Tmem26, markers of browning, to increase energy expenditure. Interestingly, genistein was also able to activate browning by a direct mechanism. Incubation of preadipocytes with genistein increased UCP1 expression as well as some biomarkers of browning in a concentration-dependent manner, possibly via phosphorylation of AMPK. The effect of genistein was accompanied by an increase in the number of mitochondria as well as in the maximum respiration rate of the adipocytes. In conclusion, this study indicated that genistein can increase energy expenditure by stimulating the browning process directly in preadipocytes and indirectly by increasing the circulating levels of irisin. (C) 2019 Elsevier Inc. All rights reserved.

ELSEVIER SCIENCE INC2019

Deletion of Sirt3 does not affect atherosclerosis but accelerates weight gain and impairs rapid metabolic adaptation in LDL receptor knockout mice: implications for cardiovascular risk factor development

Johan Auwerx, Chad Brokopp, Yan Liu, Julien Weber

Sirt3 is a mitochondrial NAD(+)-dependent deacetylase that governs mitochondrial metabolism and reactive oxygen species homeostasis. Sirt3 deficiency has been reported to accelerate the development of the metabolic syndrome. However, the role of Sirt3 in atherosclerosis remains enigmatic. We aimed to investigate whether Sirt3 deficiency affects atherosclerosis, plaque vulnerability, and metabolic homeostasis. Low-density lipoprotein receptor knockout (LDLR (-/-)) and LDLR/Sirt3 double-knockout (Sirt3 (-/-) LDLR (-/-)) mice were fed a high-cholesterol diet (1.25 % w/w) for 12 weeks. Atherosclerosis was assessed en face in thoraco-abdominal aortae and in cross sections of aortic roots. Sirt3 deletion led to hepatic mitochondrial protein hyperacetylation. Unexpectedly, though plasma malondialdehyde levels were elevated in Sirt3-deficient mice, Sirt3 deletion affected neither plaque burden nor features of plaque vulnerability (i.e., fibrous cap thickness and necrotic core diameter). Likewise, plaque macrophage and T cell infiltration as well as endothelial activation remained unaltered. Electron microscopy of aortic walls revealed no difference in mitochondrial microarchitecture between both groups. Interestingly, loss of Sirt3 was associated with accelerated weight gain and an impaired capacity to cope with rapid changes in nutrient supply as assessed by indirect calorimetry. Serum lipid levels and glucose tolerance were unaffected by Sirt3 deletion in LDLR (-/-) mice. Sirt3 deficiency does not affect atherosclerosis in LDLR (-/-) mice. However, Sirt3 controls systemic levels of oxidative stress, limits expedited weight gain, and allows rapid metabolic adaptation. Thus, Sirt3 may contribute to postponing cardiovascular risk factor development.

Springer Verlag2013

Deletion of Sirt3 does not affect atherosclerosis but accelerates weight gain and impairs rapid metabolic adaptation in LDL receptor knockout mice: implications for cardiovascular risk factor development

Johan Auwerx, Chad Brokopp, Yan Liu, Julien Weber

Springer Verlag2013

EPFL2022