Dehydroepiandrosterone (DHEA) and the dehydroepiandrosterone sulfate (DHEA-S) are steroids produced mainly by the adrenal cortex. There is evidence from both human and animal models suggesting beneficial effects of these steroids for obesity, diabetes mellitus, hypertension, and osteoporosis, conditions associated with the post-menopausal period. Accordingly, we hypothesized that DHEA supplementation in ovariectomized (OVX) female rats fed a high-fat diet would maintain glucose-induced insulin secretion (GSIS) and pancreatic islet function. OVX resulted in a 30% enlargement of the pancreatic islets area compared to the control rats, which was accompanied by a 50% reduction in the phosphorylation of AKT protein in the pancreatic islets. However, a short-term high-fat diet induced insulin resistance, accompanied by impaired GSIS in isolated pancreatic islets. These effects were reversed by DHEA treatment, with improved insulin sensitivity to levels similar to the control group, and with increased serine phosphorylation of the AKT protein. These data confirm the protective effect of DHEA on the endocrine pancreas in a situation of diet-induced overweight and low estrogen concentrations, a phenotype similar to that of the post-menopausal period.
Our results show that ω-3 protect pancreatic islets from alterations induced by P. In vivo FO supplementation modulates the redox state of pancreatic β-cell. Considering that in vitro effects do not involve mitochondrial superoxide production, we can speculate that this protection might involve NAD(P)H oxidase activity.
We investigated if a carbohydrate (CHO) mouth rinse may attenuate global fatigue and improve 4-km cycling time trial (TT4km) performance. After a preliminary session, cyclists (n = 9) performed a TT4km after a CHO or placebo (PLA) mouth rinse. Mean power output, time, and ratings of perceived exertion (RPE) were recorded throughout the TT4km. Twitch interpolation responses (%VA; voluntary activation and ∆Tw; delta peak twitch torque) were compared pre and post TT4km with traditional statistics and effect size (ES) analysis. Time-to-complete the 4 km and mean power output were comparable between CHO (386.4 ± 28.0 s) and PLA (385.4 ± 22.4 s). A lower central (p = 0.054) and peripheral (p = 0.02) fatigue in CHO than in PLA were suggested by an extremely-large ES in %VA (manipulation main effect: p = 0.052, d = 1.18; manipulation-by-time interaction effect: p = 0.08, d = 1.00) and an extremely, very-large ES in ∆Tw (manipulation main effect: p = 0.07, d = 0.97; time-by-manipulation interaction effect: p = 0.09, d = 0.89). The RPE increased slower in CHO than in PLA (p = 0.051; d = 0.7). The apparent reduction in global fatigue (central and peripheral) and RPESLOPE with only one CHO mouth rinse were not translated into improved TT4km performance. Further tests may be required to verify if these likely differences in global fatigue might represent an edge in the short-lasting cycling time trial performance.
Pinealectomized rats (PINX) become glucose intolerant and exhibit increased gluconeogenesis. Melatonin is known to reduce glucocorticoid (GC) secretion, but the role of GC on the glucose intolerance of PINX is not described. Here we evaluated the participation of GC in the glucose intolerance of PINX rats. Rats were subjected to pinealectomy or fictitious surgery (sham) and treated with RU486 [0,5mg/100g/5days] or vehicle 25 days after surgeries. After that, rats were subjected to glucose and pyruvate tolerance tests. Livers were used for assessment of insulin‐induced maximal AKT activation; plasma was collected for insulin and corticosterone. The experiments were conducted at the end of the light phase of the light/dark cycle. Corticosterone levels were 30% higher in PINX (p>;0.05), compared to sham. Glucose intolerance and upregulated gluconeogenesis found in PINX were reduced by 50% after treatment with RU486 (p>;0.05). Reduced insulin levels found in PINX rats were recovered by RU486. Concordantly, insulin‐induced AKT phosphorylation in PINX (that was decreased when compared to sham; p>;0.05) was also upregulated after treatment with RU486 by 40%. We concluded that glucose intolerance of PINX rats is characterized by hepatic insulin resistance and reduced insulin levels. These metabolic adaptations may be a result of increased corticosterone levels.Financial Support: FAPESP (2011/12329–1)
Despite the positive effects of DHEA supplementation observed in menopausal women and ovariectomized rats, a potential negative effect on glucose metabolism and insulin action in the late postmenopausal condition in diet-induced obese OVX rats are reported.
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