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Insulin resistance and hyperinsulinemia occur more frequently in subjects with greater visceral adiposity, but it is not known whether these metabolic abnormalities precede or follow visceral fat accumulation. We prospectively [...]

Context: Asians are at high risk for diabetes despite having a lower average body mass index (BMI) than Caucasians, yet BMI reference ranges are not population specific. Objective: To determine [...]

Previous research has explored whether obesity causes non-insulin-dependent diabetes mellitus (NIDDM). Being overweight may contribute to development of this disease, also known as adult-onset diabetes, but the research findings to date have been inconclusive. The lack of agreement between studies probably occurred because the investigators used different definitions for both obesity and diabetes. A group of Japanese-American men was divided into three categories based on level of blood sugar after drinking a glucose (sugar) solution and according to World Health Organization criteria. Of the 229 men, 79 were normal, 72 had impaired glucose tolerance (abnormally high glucose) and 78 had NIDDM. These categories form a continuum from normal to diabetic, with impaired glucose tolerance in between. On average, the men with normal blood sugar were slightly less overweight than the other two groups, but it was concluded that no clear link between obesity and diabetes existed in these subjects. When the location of fat deposits was considered, diabetic men had more fat in certain parts of the body than normal men. Abdominal fat deposits may be a risk factor for developing NIDDM, but more research is needed to demonstrate this relationship. It is emphasized that these results apply only to Japanese-American men, a group with a high rate of NIDDM.

Glucose intolerance is associated with increased risk of coronary heart disease (CHD) in Japanese-Americans, especially in men. Intra-abdominal fat, assessed by computed tomography, is increased in those with both NIDDM [...]

The hypothesis was tested that prenatal alcohol exposure disrupts developmental homeostasis, as reflected in increased dermatoglyphic fluctuating asymmetry. Twenty-two patients with fetal alcohol syndrome (FAS) and 9 with fetal alcohol effect (FAE) were matched for sex with 31 controls. On each patient, the right a–b dermal ridge count was subtracted from the left to obtain the asymmetry value. Group differences were tested by analysis of variance (ANOVA), and paired two-tailed t tests. Mean asymmetry increased from control (1.94) through FAE (2.78) to the FAS (4.00) group. Group differences were significant by ANOVA (p = 0.0066); only the FAS and control group differed by t test (p = 0.0025). The results support the hypothesis of increased decanalization of prenatal development in the presence of alcohol.

The frequency, age distribution and development of supernumerary epiphyses in the hand and foot were radiographically documented in 98 macaque fetuses and infants. Extra epiphyses were observed only on distal metacarpal 1 and metatarsal 1, and were present in 15% of a cross‐sectional sample and 20% of a longitudinal sample. They appeared coincidentally with the ossification of other secondary epiphyses of the hand and foot. Development of extra epiphyses in this species seems to be a normal phenomenon.