Variations in maternal care induce in neonatal rodents life-long changes in glucocorticoid feedback regulation of the hypothalamic-pituitary-adrenal axis. This aspect of plasticity in neuroendocrine development has not been established in primates. We assessed, in young adult squirrel monkeys, postnatal rearing effects on cortisol-induced suppression of corticotropin-releasing factor (CRF) stimulated secretion of adrenocorticotropic hormone (ACTH). Offspring of randomly bred monkeys were periodically removed from natal groups between 13 and 21 weeks of age. In two other postnatal rearing conditions, systematic differences in maternal availability were produced by manipulating the effort required of lactating mothers to successfully find food. All offspring were subsequently administered, 3-5 years later on two occasions, an intravenous ovine CRF injection preceded 60 min earlier by placebo or cortisol pretreatment. The difference between CRF-stimulated time-integrated secretion of ACTH following placebo vs cortisol pretreatment served as an index of glucocorticoid negative feedback. Difference scores were greatest in monkeys previously separated from natal groups. This finding was not attributable to significant rearing condition differences in plasma cortisol levels achieved following pretreatment with exogenous cortisol, nor plasma ACTH levels produced when the CRF injection was preceded by pretreatment with placebo. The results suggest that postnatal experiences altered glucocorticoid feedback in monkeys at least through early adulthood. This conclusion supports retrospective reports indicating that, for humans with major mood and anxiety disorders, systematic differences in glucocorticoid feedback may reflect neural mechanisms in development linking early life stress with psychopathology in adulthood.
Ribosome biogenesis has been shown to increase following resistance exercise; yet, it is currently unknown how promoter methylation and dosage of rDNA genes influence translational capacity, as well as basal and post‐exercise rDNA transcription rates in skeletal muscle. Moreover, whether ribosome biogenesis is induced in response to acute aerobic exercise is not well characterized in skeletal muscle. Healthy volunteers (n=30; 18 men and 12 women; 31 ±8 yrs, 25 ±4 kg/m2) were randomized to an acute bout of either aerobic (AE, 45 min biking, 70% VO2max) or resistance exercise (RE, 4 x 7 x 2 exercises), or control (no exercise). Skeletal muscle biopsies were obtained before and at 30 min, 3‐, 8‐and 24 hrs following the exercise session, and RNA/DNA was extracted. Ribosomal DNA transcription and rDNA copy number were assessed using qRT‐PCR. Average methylation of the rDNA promoter (−189 to +47) was investigated using the Agena massARRAY EpiTYPER. rDNA transcription at baseline was negatively associated with rDNA copy number (r=−0,44, p<0.05) but not with average rDNA promoter methylation. Total RNA was not related to rDNA copy number or degree of methylation of the promoter. RE significantly induced rDNA transcription, whereas AE and control did not. Average methylation of the rDNA promoter (mean: 23%, range: 10–35%) varied among volunteers; however, it was not influenced by exercise at any timepoint. Gene dosage of rDNA strongly correlated to fold‐change in rDNA transcription at the 24h timepoint (r=0.85, p<0.01). Transcription of the rRNA genes increased following resistance exercise but not following aerobic exercise, indicating specificity of exercise modality in stimulating ribosome biogenesis following exercise. Average rDNA promoter methylation varied between subjects but was not affected by exercise. Dosage of the rRNA genes strongly correlated to resistance exercise induced rDNA transcription suggesting the importance of rDNA copy number for ribosome biogenesis, and likely hypertrophic potential. Support or Funding Information Swedish Research Council for Sport Science (FvW); Futurum – the Academy for Health and Care, Region Jönköping County (BA)
The increasing interest in weight loss has seen a concurrent rise in the supplemental use of thermogenics to aid weight loss efforts. To date, the effectiveness and safety of supplemental proprietary blend thermogenics, in conjunction with high-protein energy-restricted diets have not been thoroughly evaluated. The purpose of this study was to investigate the efficacy of a low-calorie, high-protein diet with and without the concomitant use of a thermogenic supplement on body weight and body composition in apparently healthy females. Subjects were divided into three groups, Bizzy Diet+FitMiss Burn (BURN, N = 12), Bizzy Diet+Placebo (PLA, N = 13), and Control (CON, N = 14), and underwent two testing sessions separated by approximately 3 weeks. Resting blood pressure (BP), resting heart rate (RHR), clinical safety markers, body weight (BW), and body composition were assessed during each testing session. Repeated measures analysis of variance (ANOVA) revealed a significant effect for time relative to BW, total body fat mass (FM), leg FM, and trunk FM. Post hoc analysis revealed that the BURN and PLA groups experienced significant decreases in both BW and total body FM compared to CON (p <.05). There were no significant interactions for BP, RHR, or clinical safety markers over the course of the study. The Bizzy Diet, both with and without the addition of FitMiss Burn thermogenic, appears to be safe for short-term use and may lead to greater improvement in body composition and BW in an apparently healthy female population.
objectiveLow‐carbohydrate ketogenic diets (LCKDs) are a common modality to facilitate weight loss/control; however, the frequency of adherence needed to attain these benefits has not been adequately described. In addition, LCKDs have the propensity to elevate circulating ketone bodies, thus supplementing ketones may confer additional health benefits. The purpose of this study was to examine potential health benefits of an intermittent LCKD diet (AIM 1), and the effects of ketone salt supplementation (AIM 2).METHODSIn both AIMs groups of male Sprague‐Dawley rats (9–10 weeks of age, 300–325 g) were provided isoenergetic amounts of a LCKD (17 g/day, 5.2 kcal/g, 20.2% protein, 10.3% CHO, 69.5% fat) or a wester diet (WD) (20 g/day, 4.5 kcal/g, 15.2% protein, 42.7% CHO, 42.0% fat) for 6 weeks. For AIM 1 an additional group of rats was fed LCKD for 5 consecutive days followed by two days of WD (LCKD+WD). In AIM 2 two additional groups of rats were either fed LCD or WD, but were also given ad libitum ketone salts mixed in water, LCD+K and WD+K. In both aims, rats were housed in resistance‐loaded voluntary running wheels.RESULTSIn AIM 1, LCKD and LCKD+WD weighed 15% less, had significantly lower insulin, and triglycerides than WD (p<0.01). Additionally, omental and peri‐renal fat depots were reduced (p<0.05), and food efficiency (g mass gained/g food consumed) was reduced in the LCKD+WD group (p≤0.05). In AIM 2, terminal body masses were LCKD+K<LCKD<WD+K<WD (all differences p≤0.05). WD+K presented the highest levels of serum triglycerides (p≤0.01). Brown fat was elevated 41% in LCKD+K relative to LCKD (p≤0.01). Also, food efficiency was reduced in the LCKD+K and WD+K groups (p≤0.05).CONCLUSIONSInterestingly, AIM 1 suggests that intermittent ketogenic dieting with exercise conferred similar health benefits as strict ketogenic dieting. Additionally, AIM 2 suggests that ketone salt supplementation with exercise attenuated fat mass deposition regardless of dietary assignment.Support or Funding InformationFunding for this project was provided in large part by J.M.W. partially from discretionary laboratory funds provided by M.D.R.
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