Gastric emptying, glucose tolerance and associated hormonal changes in heroin addiction

1984 ◽  
Vol 14 (3) ◽  
pp. 521-525 ◽  
Author(s):  
A. Hamid Ghodse ◽  
J. L. Reed

SynopsisThe gastric emptying rate of 8 heroin-dependent males was measured by means of a radioactive isotope method. A simultaneous oral glucose tolerance test was carried out. The glucose response showed a low, flat curve with a delayed peak, and increased secretion of insulin and growth hormone occurred. As the gastric emptying rate proved to be normal the observed metabolic abnormalities are not due to the effect of heroin on the gastro-intestinal tract, but must be attributed to some other effect of chronic heroin administration.

2014 ◽  
Vol 306 (12) ◽  
pp. G1099-G1107 ◽  
Author(s):  
Maya Muramatsu ◽  
Tohru Hira ◽  
Arimi Mitsunaga ◽  
Eri Sato ◽  
Shingo Nakajima ◽  
...  

The calcium-sensing receptor (CaSR) is expressed in various tissues, including the gastrointestinal tract. To investigate the role of gut CaSR on glycemic control, we examined whether single oral administration of CaSR agonist peptides affected the glycemic response in rats. Glucose tolerance tests were performed under oral or duodenal administration of various CaSR agonist peptides (γGlu-Cys, protamine, and poly-d-lysine hydrobromide) in conscious rats. Involvement of CaSR was determined by using a CaSR antagonist. Signaling pathways underlying CaSR agonist-modified glycemia were investigated using gut hormone receptor antagonists. The gastric emptying rate after the administration of CaSR agonist peptides was measured by the phenol red recovery method. Oral and duodenal administration of CaSR agonist peptides attenuated glycemic responses under the oral glucose tolerance test, but the administration of casein did not. The promotive effect on glucose tolerance was weakened by luminal pretreatment with a CaSR antagonist. Treatment with a 5-HT3 receptor antagonist partially diminished the glucose-lowering effect of peptides. Furthermore, the gastric emptying rate was decreased by duodenal administration of CaSR agonist peptides. These results demonstrate that activation of the gut CaSR by peptide agonists promotes glucose tolerance in conscious rats. 5-HT3 receptor and the delayed gastric emptying rate appear to be involved in the glucose-lowering effect of CaSR agonist peptides. Thus, activation of gut CaSR by dietary peptides reduces glycemic responses so that gut CaSR may be a potential target for the improvement of postprandial glycemia.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Theodore A. Chavkin ◽  
Loc-Duyen Pham ◽  
Aleksandar Kostic

AbstractManaging postprandial glycemic response, or the increase in blood sugar following a meal, is a crucial component to maintaining healthy blood sugar in patients with diabetes. To test whether oral probiotics can impact postprandial glycemic response, E. coli Nissle 1917 (EcN) was evaluated in an oral glucose tolerance test. Oral gavage of EcN concurrent with a glucose bolus reduced the post-gavage glycemic response in mice. However, there was no difference in glycemic response when comparing EcN to a mutant deficient in glucose metabolism. This suggests that while EcN can alter glycemic response to a glucose bolus, this effect is not mediated by direct uptake of glucose. Of the possible indirect effects EcN could have, gastric emptying rate was highlighted as a likely cause, but EcN had no effect on gastric emptying rate in mice. This leaves many more possible indirect explanations for the interaction between EcN and host glucose metabolism to be explored in future work.


2015 ◽  
Vol 100 (9) ◽  
pp. 3565-3571 ◽  
Author(s):  
Chinmay S. Marathe ◽  
Michael Horowitz ◽  
Laurence G. Trahair ◽  
Judith M. Wishart ◽  
Michelle Bound ◽  
...  

Diabetes Care ◽  
2016 ◽  
Vol 39 (8) ◽  
pp. 1431-1439 ◽  
Author(s):  
Joon Young Kim ◽  
Sara F. Michaliszyn ◽  
Alexis Nasr ◽  
SoJung Lee ◽  
Hala Tfayli ◽  
...  

2020 ◽  
Vol 23 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Christine Dalgård ◽  
Soren Möller ◽  
Kirsten O. Kyvik

AbstractType 2 diabetes, which is caused by both genetic and environmental factors, may be diagnosed using the oral glucose tolerance test (OGTT). Recent studies demonstrated specific patterns in glucose curves during OGTT associated with cardiometabolic risk profiles. As the relative contribution of genetic and environmental influences on glucose curve patterns is unknown, we aimed to investigate the heritability of these patterns. We studied twins from the Danish GEMINAKAR cohort aged 18–67 years and free from diabetes at baseline during 1997–2000; glucose concentrations were measured three times during a 2-h OGTT. Heterogeneity of the glucose response during OGTT was examined with latent class mixed-effects models, evaluating goodness of fit by Bayes information criterion. The genetic influence on curve patterns was estimated using quantitative genetic modeling based on linear structural equations. Overall, 1455 twins (41% monozygotic) had valid glucose concentrations measured from the OGTT, and four latent classes with different glucose response patterns were identified. Statistical modeling demonstrated genetic influence for belonging to a specific class or not, with heritability estimated to be between 45% and 67%. During ∼12 years of follow-up, the four classes were each associated with different incidence of type 2 diabetes. Hence, glucose response curve patterns associated with type 2 diabetes risk appear to be moderately to highly heritable.


Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2446
Author(s):  
Rebecca O’Rielly ◽  
Hui Li ◽  
See Meng Lim ◽  
Roger Yazbeck ◽  
Stamatiki Kritas ◽  
...  

Chronic isoleucine supplementation prevents diet-induced weight gain in rodents. Acute-isoleucine administration improves glucose tolerance in rodents and reduces postprandial glucose levels in humans. However, the effect of chronic-isoleucine supplementation on body weight and glucose tolerance in obesity is unknown. This study aimed to investigate the impact of chronic isoleucine on body weight gain and glucose tolerance in lean and high-fat-diet (HFD) induced-obese mice. Male C57BL/6-mice, fed a standard-laboratory-diet (SLD) or HFD for 12 weeks, were randomly allocated to: (1) Control: Drinking water; (2) Acute: Drinking water with a gavage of isoleucine (300 mg/kg) prior to the oral-glucose-tolerance-test (OGTT) or gastric-emptying-breath-test (GEBT); (3) Chronic: Drinking water with 1.5% isoleucine, for a further six weeks. At 16 weeks, an OGTT and GEBT was performed and at 17 weeks metabolic monitoring. In SLD- and HFD-mice, there was no difference in body weight, fat mass, and plasma lipid profiles between isoleucine treatment groups. Acute-isoleucine did not improve glucose tolerance in SLD- or HFD-mice. Chronic-isoleucine impaired glucose tolerance in SLD-mice. There was no difference in gastric emptying between any groups. Chronic-isoleucine did not alter energy intake, energy expenditure, or respiratory quotient in SLD- or HFD-mice. In conclusion, chronic isoleucine supplementation may not be an effective treatment for obesity or glucose intolerance.


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