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Objective: The aim of this study was to determine the influence of a gas exchange correction protocol on resting metabolic rate (RMR) and respiratory quotient (RQ), assessed by a Vmax Encore 29n metabolic cart (SensorMedics Co., Yorba Linda, California) in overnight fasted and fed humans, and to assess the predictive power of body size for corrected and uncorrected RMR.Methods: Healthy participants (23 M/29 F; 34 ± 9 years old; 26.3 ± 3.7 kg/m2 ) ingested two 3-hour-apart glucose loads (75 g). Indirect calorimetry was conducted before and hourly over a 6-hour period. Immediately after indirect calorimetry assessment, gas exchange was simulated through high-precision mass-flow regulators, which permitted the correction of RMR and RQ values.Results: Uncorrected and corrected RMR and RQ were directly related at each time over the 6-hour period. However, uncorrected versus corrected RMR was 6.9% ± 0.5% higher (128 ± 7 kcal/d; P < 0.0001), while RQ was 14.0 ± 0.4% lower (-0.114 ± 0.003; P < 0.0001) when compared throughout the whole period. Body weight, sex, and age explained a larger fraction of the variance when corrected RMR was considered (adjusted R2  = 0.71; P < 0.0001) versus uncorrected RMR (adjusted R2  = 0.59; P < 0.0001).Conclusions: Applying a protocol to correct gas exchange in humans over a 6-hour period is feasible and provides information of improved accuracy. [ABSTRACT FROM AUTHOR]

The overexpression of the adipose gene ( adp/WDTC1) in mice inhibits lipid accumulation and improves the metabolic profile. Objective Subcutaneous fat adp expression in humans and its relation to metabolic parameters was evaluated. Design and Methods Abdominal subcutaneous fat adp expression, insulin sensitivity (clamp), and respiratory quotient (RQ; indirect calorimetry) were assessed in: 36 obese and 56 BMI-, race-, and sex-matched type 2 diabetic volunteers (Look AHEAD Adipose Ancillary Study); 37 nondiabetic Pima Indians including obese ( n = 18) and nonobese ( n = 19) subjects and; 62 nonobese nondiabetic subjects at the Pennington Center in the ADAPT study. Results In the Look AHEAD Study, adp expression normalized for cyclophilin B was higher in males versus females (1.27 ± 0.06 vs. 1.11 ± 0.04; P < 0.01) but not after controlling for body fat. Adp expression was not influenced by the presence of diabetes but was related to body fat ( r = −0.23; P = 0.03), insulin sensitivity ( r = 0.23; P = 0.03) and fasting/insulin-stimulated RQ ( r = 0.31 and 0.33; P < 0.01). In Pima Indians, adp expression was also higher in males versus females (1.00 ± 0.05 vs. 0.77 ± 0.05; P = 0.02) and higher in nonobese versus obese (1.02 ± 0.05 vs. 0.80 ± 0.06; P = 0.03). In the ADAPT study, there was no difference in adp expression between males and females. Conclusion Consistent with animal studies, our results suggest that high adp expression in human adipose tissue is associated with lower adiposity and enhanced glucose utilization. [ABSTRACT FROM AUTHOR]

Reduced skeletal muscle mitochondrial density is proposed to lead to impaired muscle lipid oxidation and increased lipid accumulation in sedentary individuals. We assessed exercise-stimulated lipid oxidation by imposing a prolonged moderate-intensity exercise in men with variable skeletal muscle mitochondrial density as measured by citrate synthase (CS) activity. After a 2-day isoenergetic high-fat diet, lipid oxidation was measured before and during exercise (650 kcal at 50% VO2max) in 20 healthy men with either high (HI-CS = 24 ± 1; mean ± s.e.) or low (LO-CS = 17 ± 1 nmol/min/mg protein) muscle CS activity. Vastus lateralis muscle biopsies were obtained before and immediately after exercise. Respiratory exchange data and blood samples were collected at rest and throughout the exercise. HI-CS subjects had higher VO2max (50 ± 1 vs. 44 ± 2 ml/kg fat free mass/min; P = 0.01), lower fasting respiratory quotient (RQ) (0.81 ± 0.01 vs. 0.85 ± 0.01; P = 0.04) and higher ex vivo muscle palmitate oxidation (866 ± 168 vs. 482 ± 78 nmol/h/mg muscle; P = 0.05) compared to LO-CS individuals. However, whole-body exercise-stimulated lipid oxidation (20 ± 2 g vs. 19 ± 1 g; P = 0.65) and plasma glucose, lactate, insulin, and catecholamine responses were similar between the two groups. In conclusion, in response to the same energy demand during a moderate prolonged exercise bout, reliance on lipid oxidation was similar in individuals with high and low skeletal muscle mitochondrial density. This data suggests that decreased muscle mitochondrial density may not necessarily impair reliance on lipid oxidation over the course of the day since it was normal under a high-lipid oxidative demand condition. Twenty-four-hour lipid oxidation and its relationship with mitochondrial density need to be assessed. [ABSTRACT FROM AUTHOR]

Insulin sensitivity (IS) is measured by the euglycemic–hyperinsulinemic clamp under a nonphysiological condition. Daily C-peptide urinary excretion may be a physiological index of IS, because C-peptide is co-secreted with insulin as a function of nutrient intake and IS. The amount of 2H2O released from glycolytic glucose metabolism after [6,6-2H2]-glucose ingestion was recently proposed as a physiological measure of IS. We compared these IS surrogates to the gold standard (euglycemic–hyperinsulinemic clamp). Thirty (15 male/15 female) sedentary, nondiabetic participants (27.2 ± 4.0 (s.d.) kg/m2, 35 ± 12 years) were admitted for 3 days to our in-patient unit. After a 10-h fast, they received 60 g of glucose and 15 g of [6,6-2H2]-glucose. Before glucose ingestion and hourly thereafter for 4 h, plasma glucose and insulin concentrations, and plasma deuterium enrichment were determined. Plasma 2H2O production divided by insulin response was used as the glycolytic index. On day 2, subjects spent 23 h in a metabolic chamber (eucaloric diet, 50% carbohydrate, 30% fat). Urinary C-peptide excretion was divided by energy intake yielding the C-peptide to energy intake ratio (CPEP/EI). After leaving the chamber (day 3, 10-h fast), IS was measured by a 2-h clamp (120 mU/m2/min). Average IS (clamp) was 7.3 ± 2.6 mg glucose/kg estimated metabolic body size/min (range: 3.6–13.2). These values were inversely correlated with CPEP/EI (r = −0.62; P < 0.01) and positively with the glycolytic rate (r = 0.60; P < 0.01). In nondiabetic subjects, two novel estimates of IS—daily urinary C-peptide urinary excretion and glycolytic rate during an oral glucose tolerance test —were related to IS by a clamp. [ABSTRACT FROM AUTHOR]

In the article, the author discusses analytical and conceptual aspects of metabolic adaptations and mentions ways to prevent excessive weight loss. Topics discussed include dependence of Metabolic rate on body's size of fat and fat-free masses with a specific percentage of resting thermogenesis, residual analysis which is a method for controlling thermogenesis for a body size, weight loss-induced metabolic adaptation due to negative residual value and high-metabolic-rate organs of obese people.

The authors reflect on the results of a study that appeared in the journal "Obesity" which examined the effect of visceral fat on insulin resistance in the canine model. They explain that the study considered the effect of increasing canine ornamental fat through pharmacological sympathectomy on insulin sensitivity and found that visceral fat per se does not result in insulin resistance. They argue that the results may not be suitable for testing the portal hypothesis.