Although T cells bearing yv T-cell receptors have long been known to be present in the epithelial lining of many organs, their specificity and function remain elusive. In the present study, we examined the intestinal epithelia of T-cell-receptor mutant mice, which were deficient in either yS T cells or ca3 T cells, and of normal littermates. The absence of yS T cells was associated with a reduction in epithelial cell turnover and a downregulation of the expression of major histocompatibility complex class II molecules. No such effects were observed in a38 T-cell-deficient mice. These findings indicate that intraepithelial yeS T cells regulate the generation and differentiation of intestinal epithelial cells.

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Hepatocyte growth factor (HGF) is one of the adipocytokines. We evaluated whether serum levels of HGF are related to the metabolic syndrome. A total of 1474 subjects of a general population free of liver, kidney, and lung diseases received a health examination. We measured blood pressure, waist circumference, body mass index, fasting plasma glucose, lipid profiles, serum insulin, liver enzymes, and HGF concentrations. Uni- and multivariate analyses for determinant of HGF were performed. In univariate analysis, all of the components (waist circumference, triglycerides, high-density lipoprotein-cholesterol, blood pressure, and fasting plasma glucose) of the metabolic syndrome and liver enzymes were significantly related to HGF levels. By the use of multiple stepwise regression analysis, HGF levels were significantly related to waist circumference (P < 0.001), high-density lipoprotein-cholesterol (P < 0.05, inversely), and liver enzymes (P < 0.001). HGF levels were higher (P < 0.05) in proportion to the accumulation of the number of the component of the metabolic syndrome. A significant association (P < 0.05) was shown between quartiles of HGF levels and the degree of abnormality of the component of the metabolic syndrome. In conclusion, our results indicate that serum HGF levels are strongly associated with the metabolic syndrome, independent of liver function.

Although it has been suggested that alcohol intake is related to hypertension, few long-term prospective studies have investigated this relationship. We therefore conducted a prospective study in male residents of a farming community in Japan to determine whether heavy drinking would predispose to the development of hypertension. A total of 325 normotensive (< 140/90 mm Hg) men were enrolled in 1977. Twelve years later, 93 (28.6%) subjects became hypertensive (defined as blood pressure > or = 140/90 mm Hg or use of antihypertensive medication). The probability of the development of hypertension in heavy drinkers predicted from a logistic regression equation was 44.6% (relative risk: 2.05 versus nondrinkers) after adjusting for age and body mass index (BMI). It was 36.2% (relative risk: 1.86 versus nondrinkers) after a further adjustment for systolic blood pressure at baseline. A high odds ratio of 2.39 for the development of hypertension with alcohol intake of < 46 g/day versus > or = 46 g/day at baseline was obtained even after adjustments for age, BMI, and confounding factors. We conclude that habitual heavy drinking of alcohol is a risk factor for the development of hypertension. This is the first report demonstrating a significant relationship between habitual alcohol intake and the development of hypertension in a long-term prospective study in Japan.