Resting energy expenditure in adolescents with Down syndrome: a comparison of commonly used predictive equations.

BACKGROUND: Adolescents with Down syndrome (DS) are two to three times more likely to be obese than their typically developing peers. When preventing or treating obesity, it is useful for clinicians to understand an individual's energy intake needs. Predictive resting energy expenditure (REE) equations are often recommended for general use in energy intake recommendations; however, these predictive equations have not been validated in youth with DS. The aim of this study was to compare the accuracy of seven commonly used predictive equations for estimating REE in adolescents who are typically developing to REE measured by indirect calorimetry in adolescents with DS. METHODS: Adolescents with DS participated in a 90-min laboratory visit before 10:00 a.m. after a 12-h overnight fast and a 48-h abstention from aerobic exercise. REE was measured via indirect calorimetry, and estimated REE was derived using the Institute of Medicine, Molnar, Muller and World Health Organization equations. Mean differences between the measured and predicted REE for each equation were evaluated with equivalency testing, and P-values were adjusted for multiple comparisons using the Holm method. RESULTS: Forty-six adolescents with DS (age: 15.5 ± 1.7 years, 47.8% female, 73.9% non-Hispanic White) completed the REE assessment. Average measured REE was 1459.5 ± 267.8 kcal/day, and the Institute of Medicine equations provided the most accurate prediction of REE with a 1.7 ± 11.2% (13.9 ± 170.3 kcal/day) overestimation. This prediction was not statistically different from the measured REE [P-value = 0.582; 95% confidence interval (CI): -64.5, 36.7], and the difference between the measured and predicted REE was statistically equivalent to zero (P-value = 0.024; 90% CI: -56.1, 28.3). CONCLUSIONS: The results suggest that the Institute of Medicine equation may be useful in predicting REE in adolescents with DS. Future research should confirm these results in a larger sample and determine the utility of the Institute of Medicine equation for energy intake recommendations during a weight management intervention.

Gut microbiota are linked to increased susceptibility to hepatic steatosis in low-aerobic-capacity rats fed an acute high-fat diet.

Poor aerobic fitness is linked to nonalcoholic fatty liver disease and increased all-cause mortality. We previously found that rats with a low capacity for running (LCR) that were fed an acute high-fat diet (HFD; 45% kcal from fat) for 3 days resulted in positive energy balance and increased hepatic steatosis compared with rats that were highly aerobically fit with a high capacity for running (HCR). Here, we tested the hypothesis that poor physiological outcomes in LCR rats following acute HFD feeding are associated with alterations in cecal microbiota. LCR rats exhibited greater body weight, feeding efficiency, 3 days of body weight change, and liver triglycerides after acute HFD feeding compared with HCR rats. Furthermore, compared with HCR rats, LCR rats exhibited reduced expression of intestinal tight junction proteins. Cecal bacterial 16S rDNA revealed that LCR rats had reduced cecal Proteobacteria compared with HCR rats. Microbiota of HCR rats consisted of greater relative abundance of Desulfovibrionaceae and unassigned genera within this family, suggesting increased reduction of endogenous mucins and proteins. Although feeding rats an acute HFD led to reduced Firmicutes in both strains, short-chain fatty acid-producing Phascolarctobacterium was reduced in LCR rats. In addition, Ruminococcae and Ruminococcus were negatively correlated with energy intake in the LCR/HFD rats. Predicted metagenomic function suggested that LCR rats had a greater capacity to metabolize carbohydrate and energy compared with HCR rats. Overall, these data suggest that the populations and metabolic capacity of the microbiota in low-aerobically fit LCR rats may contribute to their susceptibility to acute HFD-induced hepatic steatosis and poor physiologic outcomes.

The influence of reduced insulin sensitivity via short-term reductions in physical activity on cardiac baroreflex sensitivity during acute hyperglycemia.

Reduced insulin sensitivity and impaired glycemic control are among the consequences of physical inactivity and have been associated with reduced cardiac baroreflex sensitivity (BRS). However, the effect of reduced insulin sensitivity and acute hyperglycemia following glucose consumption on cardiac BRS in young, healthy subjects has not been well characterized. We hypothesized that a reduction in insulin sensitivity via reductions in physical activity would reduce cardiac BRS at rest and following an oral glucose tolerance test (OGTT). Nine recreationally active men (23 ± 1 yr; >10,000 steps/day) underwent 5 days of reduced daily physical activity (RA5) by refraining from planned exercise and reducing daily steps (<5,000 steps/day). Spontaneous cardiac BRS (sequence technique) was compared at rest and for 120 min following an OGTT at baseline and after RA5. A substudy (n = 8) was also performed to independently investigate the influence of elevated insulin alone on cardiac BRS using a 120-min hyperinsulinemic-euglycemic clamp. Insulin sensitivity (Matsuda index) was significantly reduced following RA5 (BL 9.2 ± 1.3 vs. RA5 6.4 ± 1.1, P < 0.001). Resting cardiac BRS was unaffected by RA5 and significantly reduced during the OGTT similarly at baseline and RA5 (baseline 0 min, 28 ± 4 vs. 120 min, 18 ± 4; RA5 0 min, 28 ± 4 vs. 120 min, 21 ± 3 ms/mmHg). Spontaneous cardiac BRS was also reduced during the hyperinsulinemic-euglycemic clamp (P < 0.05). Collectively, these data demonstrate that acute elevations in plasma glucose and insulin can impair spontaneous cardiac BRS in young, healthy subjects, and that reductions in cardiac BRS following acute hyperglycemia are unaffected by reduced insulin sensitivity via short-term reductions in physical activity.

Sex-dependent effects of developmental exposure to bisphenol A and ethinyl estradiol on metabolic parameters and voluntary physical activity.

Endocrine disrupting chemicals (EDC) have received considerable attention as potential obesogens. Past studies examining obesogenic potential of one widespread EDC, bisphenol A (BPA), have generally focused on metabolic and adipose tissue effects. However, physical inactivity has been proposed to be a leading cause of obesity. A paucity of studies has considered whether EDC, including BPA, affects this behavior. To test whether early exposure to BPA and ethinyl estradiol (EE, estrogen present in birth control pills) results in metabolic and such behavioral disruptions, California mice developmentally exposed to BPA and EE were tested as adults for energy expenditure (indirect calorimetry), body composition (echoMRI) and physical activity (measured by beam breaks and voluntary wheel running). Serum glucose and metabolic hormones were measured. No differences in body weight or food consumption were detected. BPA-exposed females exhibited greater variation in weight than females in control and EE groups. During the dark and light cycles, BPA females exhibited a higher average respiratory quotient than control females, indicative of metabolizing carbohydrates rather than fats. Various assessments of voluntary physical activity in the home cage confirmed that during the dark cycle, BPA and EE-exposed females were significantly less active in this setting than control females. Similar effects were not observed in BPA or EE-exposed males. No significant differences were detected in serum glucose, insulin, adiponectin and leptin concentrations. Results suggest that females developmentally exposed to BPA exhibit decreased motivation to engage in voluntary physical activity and altered metabolism of carbohydrates v. fats, which could have important health implications.

A pilot study examining the effects of consuming a high-protein vs normal-protein breakfast on free-living glycemic control in overweight/obese 'breakfast skipping' adolescents.

To examine whether the daily consumption of normal-protein (NP) vs higher-protein (HP) breakfasts improve free-living glycemic control in overweight/obese, 'breakfast skipping' adolescents. Twenty-eight healthy, but overweight, teens (age: 19±1 year; BMI: 29.9±0.8 kg m(-2)) completed a 12-week randomized parallel-arm study in which the adolescents consumed either a 350 kcal NP breakfast (13 g protein) or HP breakfast (35 g protein). Pre- and post-study 24-h blood glucose measures were assessed using continuous glucose monitoring. Although no main effects of time or group were detected, time by group interactions were observed. Post hoc pairwise comparisons assessing the post-pre changes revealed that the daily consumption of the HP breakfasts tended to reduce the 24-h glucose variability (s.d.) vs NP (-0.17±0.09 vs +0.09±0.10 s.d.; P=0.06) and tended to reduce the time spent above the high glucose limit (-292±118 vs -24±80 min; P=0.09). The consumption of the HP breakfasts also reduced the 24-h maximal (peak) glucose response (-0.94±0.36 vs +0.30±0.18 mmol l(-1); P<0.01) and reduced postprandial glucose fluctuations (-0.88±0.44 vs +0.49±0.34 mmol l(-1); P<0.03) vs NP. These data suggest that the daily addition of a HP breakfast, containing 35 g of high-quality protein, has better efficacy at improving free-living glycemic control compared with a NP breakfast in overweight/obese, but otherwise healthy, 'breakfast skipping' adolescents.

The effect of breakfast type and frequency of consumption on glycemic response in overweight/obese late adolescent girls.

BACKGROUND/OBJECTIVES: The primary aim was to examine the daily glycemic response to normal-protein (NP) vs higher-protein (HP) breakfasts in overweight adolescents who habitually skip breakfast (H-BS). The secondary aim examined whether the glycemic response to these meals differed in H-BS vs habitual breakfast consumers (H-BC). SUBJECTS/METHODS: Thirty-five girls (age: 19 ± 1 year; body mass index: 28.4 ± 0.7 kg/m(2)) participated in the semi-randomized crossover-design study. The participants were grouped according to habitual breakfast frequency. H-BS (n = 20) continued to skip breakfast (BS) or consumed a NP (12 g protein) or HP (32 g protein) breakfast for 3 days, whereas the H-BC (n = 15) completed the NP and HP breakfast conditions for 3 days. On day 4 of each pattern, an 8 h testing day was completed. The respective breakfast and a standard lunch meal were provided, and plasma was collected to assess morning, afternoon, and total glucose and insulin area under the curves (AUC). RESULTS: In H-BS, the addition of a HP breakfast increased total glucose AUC vs BS (P < 0.05), whereas NP breakfast increased total insulin AUC vs BS (P < 0.05). In H-BC, the HP breakfast reduced morning, afternoon and total glucose AUCs vs NP (all, P < 0.05). No differences in insulin were detected. When comparing the HP-NP differential glycemic responses between groups, H-BS experienced greater afternoon and total glucose AUCs following HP vs NP breakfasts (both, P<0.05). No differences in insulin responses were observed between groups. CONCLUSIONS: Novel differences in the glucose response to HP vs NP breakfasts were observed and were influenced by the frequency of habitual breakfast consumption in overweight adolescents.

Type 2 diabetes sits in a chair.

The incidence of type 2 diabetes (T2D) continues to skyrocket across the industrialized world leading to soaring medical costs, reduced quality of life and increased mortality rates. Therefore, a more firm understanding of the development of the disease and effective, low cost therapies for prevention and treatment are desperately needed. Accumulating evidence suggests that increased sedentary time (i.e. 'sitting time') combined with reduced physical activity levels, plays both a major role in the development of T2D and may contribute to the worsening of the condition after diagnosis. In this review, we cover these topics and use current scientific evidence to support our belief that 'type 2 diabetes sits in a chair'. We also discuss a relatively new question that has yet to be examined: Would reducing sitting time be an effective treatment for T2D?

Glycaemic control is improved by 7 days of aerobic exercise training in patients with type 2 diabetes.

AIMS/HYPOTHESIS: Cardiovascular events and death are better predicted by postprandial glucose (PPG) than by fasting blood glucose or HbA(1c). While chronic exercise reduces HbA(1c) in patients with type 2 diabetes, short-term exercise improves measures of insulin sensitivity but does not consistently alter responses to the OGTT. The purpose of this study was to determine whether short-term exercise training improves PPG and glycaemic control in free-living patients with type 2 diabetes, independently of the changes in fitness, adiposity and energy balance often associated with chronic exercise training. METHODS: Using continuous glucose monitors, PPG was quantified in previously sedentary patients with type 2 diabetes not using exogenous insulin (n = 13, age 53 ± 2 years, HbA(1c) 6.6 ± 0.2% (49.1 ± 1.9 mmol/mol)) during 3 days of habitual activity and during the final 3 days of a 7 day aerobic exercise training programme (7D-EX) which does not elicit measurable changes in cardiorespiratory fitness or body composition. Diet was standardised across monitoring periods, with modifications during 7D-EX to offset increases in energy expenditure. OGTTs were performed on the morning following each monitoring period. RESULTS: 7D-EX attenuated PPG (p < 0.05) as well as the frequency, magnitude and duration of glycaemic excursions (p < 0.05). Conversely, average 24 h blood glucose did not change, nor did glucose, insulin or C-peptide responses to the OGTT. CONCLUSIONS/INTERPRETATION: 7D-EX attenuated glycaemic variability and PPG in free-living patients with type 2 diabetes but did not significantly alter responses to the laboratory-based OGTT. These effects appeared to be independent of changes in fitness, body composition or energy balance. ClinicalTrials.gov numbers: NCT00954109 and NCT00972452. FUNDING: This project was funded by the University of Missouri Institute for Clinical and Translational Sciences (CRM), NIH grant T32 AR-048523 (CRM), Diabetes Action Research and Education Foundation (JPT). Medtronic supplied CGMS sensors at a discounted rate.

Effects of acute pinitol supplementation on plasma pinitol concentration, whole body glucose tolerance, and activation of the skeletal muscle insulin receptor in older humans.

Limited research with rodents and humans suggests that oral ingestion of pinitol (3- O-methyl- D- CHIRO-inositol) might positively influence glucose tolerance. This double-blinded, placebo-controlled, and cross-over study assessed the effects of acute pinitol supplementation on plasma pinitol concentration, glucose tolerance, insulin sensitivity, and activation of the skeletal muscle insulin receptor. Fifteen older, nondiabetic subjects (62+/-1 years, mean+/-SEM) completed four, 1-day trials. Subjects consumed a non-nutritive beverage with nothing (placebo) or 1,000 mg pinitol. Sixty minutes later, the subjects consumed beverages that were either energy- and carbohydrate-free (Sham) or contained 75 g glucose (OGTT). Blood samples were collected frequently over the 240-min testing period. For the OGTT trials only, vastus lateralis samples were obtained before the placebo and pinitol supplementation and 60 min after consuming the 75 g glucose beverage. Plasma pinitol concentration increased and was maintained for 240 min. Pinitol did not influence the fasting state and 180-min area under the curves for plasma glucose and insulin during the Sham and OGTT trials or hepatic (placebo 0.83+/-0.08; pinitol 0.80+/-0.08) and whole-body (placebo 6.10+/-0.54; pinitol 6.22+/-0.52) insulin sensitivities. Activation of the muscle insulin receptor was increased by 140% with glucose ingestion (Pre 0.62+/-0.12; Post 1.49+/-0.35), but pinitol did not influence this response. These results show that the pinitol supplement was quickly absorbed, but did not acutely influence indices of whole-body glucose tolerance and insulin sensitivity, or the activation of the skeletal muscle insulin receptor in older, nondiabetic humans.