BACKGROUND: Despite the westernized lifestyle, most Japanese are not prominently obese. As their obesity may be obscured, we want to further explore central fat distribution and health risks among this population. METHODS: 2668 men (body mass index (BMI) 20 ±`26.4 kgam 2 ) were identi®ed from 3343 men (BMI 14.0 ± 37.7, median of waist-to-height ratio (WaHt) 0.50) who underwent routine health examinations. They were divided into four groups: (1) BMI 20 ±`24, WaHt`0.50; (2) BMI 20 ±`24, WaHt ! 0.50; (3) BMI 24 ±`26.4, WaHt`0.50; and (4) BMI 24 ± 26.4, WaHt ! 0.50. The metabolic risks and physical activities were compared. RESULTS: WaHt ! 0.50 comprised 35% of the subjects of BMI 20 ±`24, 91% of BMI 24 ±`26.4, only 1% of BMI`20 and up to 99% of BMI ! 26.4. After adjusting for age and smoking and with group 1 as the reference group, odds ratios (ORs) were signi®cantly higher in both groups 2 and 4 for the risk of hypertension (1.42, 1.98), hyperglycaemia (1.49, 1.78), hypertriglyceridaemia (1.95, 2.56), low HDL cholesterol (1.87, 2.20), hyperuricaemia (2.00, 2.51) and fatty liver (2.57, 5.64) and additionally in group 4 for hypercholesterolaemia (1.35). ORs in group 3 were only signi®cantly higher for risk of hypertension (1.86) and fatty liver (1.89). Signi®cantly lower frequencies of regular physical activity were noted in the higher WaHt groups (0.75, 0.47, 1.10, 0.52 days per week, from groups 1 ± 4, respectively). CONCLUSIONS: Measurement of waist circumference may be a preliminary method for the survey of people at higher risk of lifestyle-related disorders in Japanese men, especially among those with moderate BMI.

The results imply that OTX2 mutations are associated with variable pituitary phenotype, with no genotype-phenotype correlations, and that OTX2 can transactivate GNRH1 as well as HESX1 and POU1F1.

This study demonstrated the characteristic association of HLA-class II and class I genes with Type 1A diabetes among Japanese children. A TDT did not reveal the genomic imprinting of HLA-class II and class I genes in Type 1A diabetes.

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BackgroundMiglitol is an oral anti-diabetic drug that acts by inhibiting carbohydrate absorption in the small intestine. Recent studies have shown that miglitol reduces obesity in humans and rodents. However, its mechanisms have remained unclear. The purpose of this study was to determine whether miglitol generates heat by activating uncoupling protein 1 (UCP1), an enzyme involved in thermogenesis, in brown adipose tissue (BAT) in mice.MethodsFour-week-old male C57BL/6 J mice were fed a high-fat diet alone (HF) or a high fat diet plus miglitol (HFM). Oxygen consumption (VO2) was used to estimate metabolic rate. A thermal imaging camera was used to quantify heat generation from interscapular brown adipose tissue. We analyzed the protein and gene expressions of UCP1 and the expressions of four proteins related to β3-adrenergic signaling in the pathway activating UCP1 (protein kinase A (PKA), hormone-sensitive lipase (HSL), p38 α mitogen-activated protein kinase (p38αMAPK) and peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α)).ResultsAt 8 weeks, body weight, epididymal and subcutaneous white adipose tissue and the HOMA-R value of the HFM mice were significantly less than those of the HF mice. Food intake was not different between the HF and HFM mice. VO2 and BAT temperature were significantly higher in the HFM mice. Miglitol significantly enhanced the gene and protein expressions of UCP1 and the expressions of proteins related to β3-adrenergic signaling.ConclusionsMiglitol’s anti-obesity effect was attributed to increased energy expenditure by upregulating UCP1 in BAT (i.e., by thermogenesis) and to enhancement of β3-adrenergic signaling in BAT.