Search

The rate of fat oxidation at rest decreases with age in women. The mechanisms for this decrease are not clear. Theoretically, a decrease in the availability of fatty acids could explain the decline in fat oxidation. In consequence, the in vivo rate of production of fatty acids as a proxy for lipolysis was measured in 21 healthy women. Eleven of the volunteers were elderly (> 65 years) and 10 were young (< 24 years), and all were characterized for body composition. The nonadjusted rate of delivery of fatty acids into the systemic circulation was similar among elderly and young individuals (609 +/- 80.3 v 597 +/- 69.9 mumol/min, respectively, P > .1). When lipolysis was adjusted for the differences in fat-free mass using analysis of covariance (ANCOVA), rates were slightly increased in the elderly group (626 +/- 80 mumol/min) and decreased in the young group (578 +/- 84 mumol/min), but remained nonstatistically significant. It is concluded that mechanisms other than lipolysis must explain the decrease of fat oxidation in aging women, i.e., a decrease in the capacity of muscle to oxidize fat and/or a decrease in its capacity for transport of long-chain fatty acids.

The quantitative contribution of hepatic glucose cycling to basal and glucagon-stimulated thermogenesis was investigated in seven normal healthy volunteers in whom energy expenditure (EE) was measured simultaneously with indirect calorimetry. Primed-constant infusions of 2-(2H1)-glucose and 6-6'-(2H2)-glucose were used to calculate hepatic glucose cycling. Gas chromatography/mass spectrometry was used to measure the plasma enrichment of isotopes. In response to hyperglucagonemia, basal EE increased an average of 7.1% +/- 2.3% (P < .05). This thermogenic effect of glucagon was completely blunted when insulin levels were increased sevenfold over the basal concentration. Hepatic glucose cycling comprised 15% +/- 4% of basal glucose turnover and increased more than 100% in response to isolated hyperglucagonemia. The increase in liver glucose cycling was observed also when serum insulin concentrations were increased sevenfold above baseline. Thus, we were able to induce dissociation of the activation of hepatic glucose cycling and the thermogenic response induced by hyperglucagonemia. From the quantitative point of view, the thermogenic cost of the cycles was less than 1% in both the basal and stimulated state. Thus, we concluded that hepatic glucose cycles play a quantitatively minor role in EE in man.