Weight change after 20 years of age and the incidence of dyslipidemia: a cohort study of Japanese male workers.

BACKGROUND: While heavier weight is known to increase the incidence of dyslipidemia, limited data are available on the relationship between weight gain and its development. METHODS: A total of 2647 males were categorized into the following four groups according to the difference between their self-reported weight at 20 years of age and their measured weight in 1994-95: a loss of ≥5% (decrease), loss of <5% or gain of <5% (no change), gain of ≥5 to <15% (increase) and gain of ≥15% (sizable increase). They were followed up until their 2002-03 health examination. Using the 'no change' group as reference, the multivariable-adjusted odds ratio (adjusted for age, body mass index at 20 years of age, physical activity, smoking and alcohol intake) and 95% confidence interval (95% CI) for the incidence of dyslipidemia were determined using logistic regression models. RESULTS: A total of 1342 participants developed dyslipidemia during the follow-up period. The 'increase' and 'sizable increase' groups had odds ratios for the incidence of dyslipidemia of 1.97 (95% CI, 1.59-2.45) and 2.68 (2.15-3.34), respectively, demonstrating that there was a significant dose-response association between weight gain since 20 years of age and the incidence of dyslipidemia (P < 0.001 for trend). CONCLUSION: These results suggest that dyslipidemia could be prevented by avoiding weight gain in adulthood.

Ca2+-dependent activation of the malate-aspartate shuttle by norepinephrine and vasopressin in perfused rat liver.

The role of Ca2+ in stimulation of the malate-aspartate shuttle by norepinephrine and vasopressin was studied in perfused rat liver. Shuttle capacity was indexed by measuring the changes in both the rate of production of glucose from sorbitol and the ratio of lactate to pyruvate during the oxidation of ethanol. (T. Sugano et al. (1986) Amer. J. Physiol. 251, E385-E392). Asparagine (0.5 mM), but not alanine (0.5 mM) decreased the ethanol-induced responses. Norepinephrine and vasopressin had no effect on the ethanol-induced responses when the liver was perfused with sorbitol or glycerol. In the presence of 0.25 mM alanine, norepinephrine, vasopressin, and A23187 decreased the ethanol-induced responses that occurred with the increase of flux of Ca2+. In liver perfused with Ca2+-free medium, asparagine also decreased the ethanol-induced responses, but norepinephrine and vasopressin had no effect. Aminooxyacetate inhibited the effects of norepinephrine, A23187, and asparagine. Regardless of the presence or absence of perfusate Ca2+, the combination of glucagon and alanine had no effect on the ethanol-induced responses. Norepinephrine caused a decrease in levels of alpha-ketoglutarate, aspartate, and glutamate in hepatocytes incubated with Ca2+. The present data suggest that the redistribution of cellular Ca2+ may activate the efflux of aspartate from mitochondria in rat liver, resulting in an increase in the capacity of the malate-aspartate shuttle.