Respiratory Quotient Predicts Fat Mass Gain in Premenopausal Women

Abstract

High respiratory quotient (RQ) has been associated with fat mass gain in some, but not all studies. Variability among results may reflect differences in the RQ variable measured (fasting vs. 24-hour) or may be due to differences in control for factors that affect RQ, such as diet, energy balance, circulating insulin, and insulin sensitivity. The objective of this study was to determine whether different RQ values (fasting, sleeping, non-sleeping, and 24-hour) would predict change in fat mass over 2 years in obesity-prone women, controlling for diet and adjusting for energy balance, circulating insulin, and insulin sensitivity. Participants were 33 previously-overweight premenopausal women. Fasting, sleeping, non-sleeping, and 24-hour RQ values were measured during controlled-diet conditions by respiratory chamber calorimetry. Intravenous glucose tolerance tests were also performed to adjust for fasting insulin, acute insulin response to glucose, and insulin sensitivity. Over the following 2 years, changes in fat mass were tracked annually by dual energy X-ray absorptiometry. High non-sleeping RQ (NSRQ) predicted 2-year change in fat mass independently of energy balance, circulating insulin, and insulin sensitivity. This observation suggests that low postprandial fat oxidation may uniquely predispose obesity-prone individuals to accrual of adipose tissue.

Energy replacement diminishes the effect of exercise on postprandial lipemia in boys

“…While the clinical significance of our findings cannot be determined, high childhood fasting [TAG] is an independent predictor of young adult cardiovascular disease [4], and physical inactivity is associated independently with the clustering of cardiovascular disease risk factors in childhood and adolescence [41]. Furthermore, low rates of fat oxidation in adults have been implicated in the pathology of obesity [42] and Type 2 diabetes mellitus [43]. Considering childhood cardiovascular disease risk factors track into adulthood [44], interventions that improve the cardiovascular disease risk factor profile should be paediatric orientated [3].…”

Impaired oxidative capacity due to decreased CPT1b levels as a contributing factor to fat accumulation in obesity

“…This indicates that obesity or high adiposity per se is not associated with high RER values and low CPT1b levels, substantiating that the high RER and low CPT1b levels observed in the OP rats could be one of the genetic underlying and molecular factors responsible for the high level of fat accumulation in this obese phenotype. Interestingly, human studies suggest that impaired fat oxidative capacities may be an important contributor to obesity because obese individuals oxidize less fat than lean individuals (3) and fat oxidation capacities have been shown to predict body weight (13,16,37,46,58). Increased desaturase activities and SCD1 expression have been described in skeletal muscle of obese humans (20,56), whereas decreased CPT1 expression has been observed (48).…”

Physiological mechanisms underlying individual variation in tolerance of food deprivation in juvenile European sea bass, Dicentrarchus labrax

“…Thus if individuals differ in their relative use of proteins versus lipids during food deprivation, they may show different rates of mass loss for the same metabolic rate. There is evidence that such a mechanism may underlie individual variation in rates of mass loss by dieting humans (Barwell et al, 2009) and also their tendency to accumulate adipose tissue when feeding (Ellis et al, 2010). When feeding routinely in aquaculture, fasting tolerant sea bass phenotypes accumulate larger intramuscular and perivisceral lipid stores Daulé et al, 2013).…”