The sympathetic nervous system is recognized to play a role in the etiology of animal and possibly human obesity through its impact on energy expenditure and/or food intake. We, therefore, measured fasting muscle sympathetic nerve activity (MSNA) in the peroneal nerve and its relationship with energy expenditure and body composition in 25 relatively lean Pima Indian males (means±SD; 26±6 yr, 82±19 kg, 28±10% body fat) and 19 Caucasian males (29±5 yr, 81±13 kg, 24±9% body fat). 24-h energy expenditure, sleeping metabolic rate, and resting metabolic rate were measured in a respiratory chamber, whereas body composition was estimated by hydrodensitometry.Pima Indians had lower MSNA than Caucasians (23±6 vs 33±10 bursts/min, P = 0.0007). MSNA was significantly related to percent body fat in Caucasians (r = 0.55, P = 0.01) but not in Pimas. MSNA also correlated with energy expenditure adjusted for fat-free mass, fat mass, and age in Caucasians (r = 0.51, P = 0.03; r = 0.54, P = 0.02; and r = 0.53, P = 0.02 for adjusted 24-h energy expenditure, sleeping metabolic rate, and resting metabolic rate, respectively) but not in Pima Indians.In conclusion, the activity of the sympathetic nervous system is a determinant of energy expenditure in Caucasians. Individuals with low resting MSNA may be at risk for body weight gain resulting from a lower metabolic rate. A low resting MSNA and the lack of impact of MSNA on metabolic rate might play a role in the etiology of obesity in Pima Indians. (J.

BACKGROUND: 24-h energy expenditure (24-EE) and 24-h respiratory quotient (24-RQ) are important measurements in obesity research, but their accurate assessment is limited to few specialized laboratories. OBJECTIVES: 1) To provide comprehensive prediction equations for 24-EE, sleeping metabolic rate (SMR) and 24-RQ, based on a large number of Caucasian and Pima Indian subjects, covering a wide range of body weight and composition, body fat distribution, and age and 2) to test whether Pima Indians have lower metabolic rate andaor higher 24-RQ than Caucasians. SUBJECTS AND METHODS: 916 non-diabetic subjects, aged 31.5 AE 11.9 y, body weight 90.5 AE 26.1 kg (mean AE s.d.), (561 males, 355 females; 416 Caucasians, 500 Pima Indians; 720 with normal (NGT) and 196 with impaired (IGT) glucose tolerance) spent 24 h in a respiratory chamber for measurements of 24-EE, SMR and 24-RQ. Fat-free mass (FFM) and fat mass (FM) were assessed by either hydrodensitometry or DEXA. Waist circumference and waist-to-thigh ratio (WTR) were determined as measures of body fat distribution. RESULTS: In a stepwise multiple regression analysis, FFM, FM, sex, age, WTR, and ethnicity were signi®cant independent determinants of 24-EE (2258 AE 422 kcalad), explaining 85% of its variability (24-EE (kcalad) 696 18.9 FFM (kg) 10.0 FM (kg) 180 male 7 1.9 age (y) 7.1 WTR (per decimal) 44 Pima Indian). SMR (1623 AE 315 kcalad) was determined (78% of variability) by FFM, FM, sex, age, WTR, and glucose tolerance (SMR (kcalad) 443 14.6 FFM (kg) 6.9 FM (kg) 79 male 7 1.0 age (y) 5.8 WTR (per decimal) 38 IGT), but not by ethnicity. Adjustment for the respective variables reduced the variance in 24-EE from 422 to 162 kcalad and in SMR from 315 to 146 kcalad. 24-RQ (0.854 AE 0.026) was determined by waist circumference and energy balance (24-RQ 0.88429 ± 0.00175 waist circumference (cm) 0.00004 energy balance (%)), but not by sex, ethnicity or glucose tolerance. With this equation only 13% of the variability in 24-RQ could be explained (residual variance 0.024). Compared to Caucasians, Pima Indians had higher 24-EE, but similar SMR and 24-RQ. CONCLUSIONS: This analysis provides comprehensive prediction equations for 24-EE, SMR and 24-RQ from their major known determinants. It con®rms the previous ®ndings that, even after adjustment for body composition, age, sex, ethnicity, and glucose tolerance, there is still considerable variability in energy expenditure and substrate oxidation that may, in part, be genetically determined. In adult Pima Indians, we found no evidence for lower metabolic rate or impaired fat oxidation that could explain the propensity towards obesity in this ethnic group.

Meal skipping has become an increasing trend of the modern lifestyle that may lead to obesity and type 2 diabetes. We investigated whether the timing of meal skipping impacts these risks by affecting circadian regulation of energy balance, glucose metabolism, and postprandial inflammatory responses. In a randomized controlled crossover trial, 17 participants [body mass index (in kg/m): 23.7 ± 4.6] underwent 3 isocaloric 24-h interventions (55%, 30%, and 15% carbohydrate, fat, and protein, respectively): a breakfast skipping day (BSD) and a dinner skipping day (DSD) separated by a conventional 3-meal-structure day (control). Energy and macronutrient balance was measured in a respiration chamber. Postprandial glucose, insulin, and inflammatory responses in leukocytes as well as 24-h glycemia and insulin secretion were analyzed. When compared with the 3-meal control, 24-h energy expenditure was higher on both skipping days (BSD: +41 kcal/d; DSD: +91 kcal/d; both < 0.01), whereas fat oxidation increased on the BSD only (+16 g/d; < 0.001). Spontaneous physical activity, 24-h glycemia, and 24-h insulin secretion did not differ between intervention days. The postprandial homeostasis model assessment index (+54%) and glucose concentrations after lunch (+46%) were, however, higher on the BSD than on the DSD (both < 0.05). Concomitantly, a longer fasting period with breakfast skipping also increased the inflammatory potential of peripheral blood cells after lunch. Compared with 3 meals/d, meal skipping increased energy expenditure. In contrast, higher postprandial insulin concentrations and increased fat oxidation with breakfast skipping suggest the development of metabolic inflexibility in response to prolonged fasting that may in the long term lead to low-grade inflammation and impaired glucose homeostasis. This trial was registered at clinicaltrials.gov as NCT02635139.

Since females have a greater prevalence of obesity compared with males, the question arises whether females have lower metabolic rate than males after adjusting for differences in body weight and composition. 24-h energy expenditure (24EE), basal metabolic rate (BMR), and sleeping metabolic rate (SMR) were measured in a respiratory chamber in 235 healthy, nondiabetic Caucasian subjects (114 males, 121 females). Body composition was determined by hydrodensitometry. 24EE was 124 +/-38 kcal/d (P less than 0.002) higher in males than females after adjusting for differences in fat-free mass, fat mass, and age. Spontaneous physical activity was not significantly different between males and females. Since adjusted 24EE was 106 +/-39 kcal/d (P less than 0.01) higher in females during the luteal phase of the menstrual cycle compared with females during the follicular phase, energy expenditure was analyzed in a subset (greater than 50 yr) to minimize the confounding effect of menstrual status. 24EE (160 +/-66 kcal/d; P less than 0.03), BMR (116 +/-45; P less than 0.02), and SMR (208 +/-68 kcal/d; P less than 0.005) were higher in males compared with females of the older subset after adjusting for differences in body composition, age, and activity. In summary, sedentary 24EE is approximately 5-10% lower in females compared with males after adjusting for differences in body composition, age, and activity.