NMN administration restored β cell glucose - stimulated insulin secretion and hepatic and muscle insulin sensitivity in mouse models of
induced glucose intolerance [33, 92, 93].
«The authors are confounding their conclusions by addressing all these noncaloric artificial sweeteners together,» says Brian Ratcliffe, a nutrition researcher at Robert Gordon University in Aberdeen, U.K.. That's why the title of the paper, «Artificial sweeteners
induce glucose intolerance by altering the gut microbiota,» is misleading, he says.
Unlike in type 1 diabetes, in which insulin production is limited because beta cells are destroyed, «arsenic
induces glucose intolerance through a disruption of beta - cell function that alters normal stimulus — secretion coupling,» the researchers wrote.
Read the full article, «Arsenic exposure
induces glucose intolerance and alters global energy metabolism,» published ahead of print in the American Journal of Physiology — Regulatory, Integrative and Comparative Physiology.
Not exact matches
In the current study, we found that while a high fat diet containing Plenish also
induced obesity,
glucose intolerance and fatty liver, it did not
induce insulin resistance as did the conventional soybean oil.
Despite not developing IR,
glucose intolerance can be
induced in C57BL / 6 mice fed a high sucrose diet (50 % sucrose) relative to those fed a similar diet high in corn starch from 10 — 55 weeks, which has been attributed to a reduced pancreatic insulin secretion (14).
Ghosh SS, Bie J, Wang J, Ghosh S. Oral supplementation with non-absorbable antibiotics or curcumin attenuates western diet -
induced atherosclerosis and
glucose intolerance in LDLR - / - mice — role of intestinal permeability and macrophage activation.
Oral supplementation with non-absorbable antibiotics or curcumin attenuates western diet -
induced atherosclerosis and
glucose intolerance in LDLR - / - mice — role of intestinal permeability and macrophage activation.
The study, Fish oil ameliorates trimethylamine N - oxide - exacerbated
glucose intolerance in high - fat diet - fed mice, found that in mice, dietary FO ameliorated TMAO -
induced impaired
glucose tolerance, insulin signal transduction in peripheral tissue, and adipose tissue inflammation in HFD - fed mice.
Cadmium concentrations in the kidney
induce renal dysfunction and contribute to hypertension due to sodium retention,
glucose intolerance, dyslipidemia and zinc deficiency.