Whether the contribution of inflammation to risk for chronic metabolic disease differs with ethnicity is not known. The objective of this study was to determine: (i) whether ethnic differences exist in markers of inflammation and (ii) whether lower insulin sensitivity among African Americans vs. whites is due to greater inflammatory status. Subjects were African-American (n = 108) and white (n = 105) women, BMI 27-30 kg/m 2 . Insulin sensitivity was assessed with intravenous glucose tolerance test and minimal modeling; fat distribution with computed tomography; body composition with dual-energy X-ray absorptiometry; markers of inflammation (tumor necrosis factor (TNF)-α, soluble tumor necrosis factor receptor (sTNFR)-1, sTNFR-2, C-reactive protein (CRP), and interleukin (IL)-6) with enzymelinked immunosorbent assay (ELISA). Whites had greater intra-abdominal adipose tissue (IAAT), insulin sensitivity, and concentrations of TNF-α, sTNFR-1, and sTNFR-2 than African Americans. Greater TNF-α in whites vs. African Americans was attributed to greater IAAT in whites. Among whites, but not African Americans, CRP was independently and inversely associated with insulin sensitivity, after adjusting for IAAT (r = −0.29 P < 0.05, and r = −0.13 P = 0.53, respectively). Insulin sensitivity remained lower in African Americans after adjusting for CRP (P < 0.001). In conclusion, greater IAAT among whites may be associated with greater inflammation. Insulin sensitivity was lower among African Americans, independent of obesity, fat distribution, and inflammation.

Adiponectin is inversely related to adiposity and positively correlated with insulin sensitivity (S i ). Sparse data exist on the contributions of ethnicity and body fat distribution to variance in serum adiponectin. Hypotheses tested were that adiponectin would be lower in African Americans compared with Caucasians; that adiponectin would be inversely related to central, not peripheral, fat; that adiponectin would be positively associated with S i ; and that baseline adiponectin would predict change in S i over 2 years in 150 African-American and Caucasian youth. Multiple linear regression modeling showed that adiponectin was lower in AfricanAmerican versus Caucasian children (adjusted means 10.8 ؎ 0.5 vs. 12.3 ؎ 0.5 g/ml, respectively; P < 0.05); inversely related to trunk fat (P < 0.05); and positively related to limb fat (P < 0.01). Addition of the acute insulin response to glucose to the model eliminated the significance of ethnicity. S i , which was positively related to adiponectin (P < 0.05), was lower in African Americans (P < 0.001) and girls (P < 0.05). Baseline adiponectin did not predict change in S i over 2 years. In conclusion, adiponectin was positively correlated with S i , inversely related to central fat, and positively related to peripheral fat. In addition, higher acute insulin response to glucose explained lower adiponectin among African-American children.

Maternal gestational glucose concentration was significantly associated with offspring insulin sensitivity and β-cell response independent of adiposity. These results suggest that maternal glucose may program the fetus both at the pancreas and at the level of insulin target tissues such as skeletal muscle and liver.

Prior research on the relationship between visual confrontation naming and hippocampal function has been inconclusive. The present study examined this relationship using quantitative (1)H magnetic resonance spectroscopy ((1)H-MRS) to operationalize the function of the left and right hippocampi. The 60-item Boston Naming Test (BNT) was used to measure naming. Our sample included 46 patients with medically intractable, focal mesial temporal lobe epilepsy who had been screened for all pathology other than mesial temporal sclerosis. Statistics included Pearson correlations and neural network analysis (multilayer perceptron and radial basis function). Baseline BNT performance correlated significantly with left (1)H-MRS hippocampal ratios. Thirty-six per cent of the variance in baseline BNT performance was explained by a neural network model using left and right (1)H-MRS ratios(creatine/N-acetylaspartate) as input. This was elevated to 49% when input from the right hippocampus was lesioned mathematically. In a second model, left (1)H-MRS hippocampal ratios were modelled using measures of semantic and episodic memory as input (including the BNT). Explained variance in left (1)H-MRS hippocampal ratios fell from 60.8 to 3.6% when input from BNT and another semantic memory measure was degraded mathematically. These results provide evidence that the speech-dominant hippocampus is a significant component of the overall neuroanatomical network of visual confrontation naming. Clinical and theoretical implications are explored.

OBJECTIVEIntrauterine exposure to high maternal glucose is associated with excess weight gain during childhood, but it is not clear whether the excess weight represents increased fat or lean mass. The purpose of this study was to examine the relationship between maternal glucose concentrations during pregnancy and offspring body composition. A secondary goal was to examine whether the association between maternal glucose and children’s body fat was independent of energy intake, energy expenditure, or physical activity.RESEARCH DESIGN AND METHODSChildren aged 5–10 years and their biological mothers (n = 27) were recruited. Maternal glucose concentration 1 h after a 50-g oral glucose load, used to screen for gestational diabetes mellitus at 24–28 weeks gestation, was retrieved from medical records. Children underwent dual-energy X-ray absorptiometry to measure body composition, indirect calorimetry to measure resting energy expenditure (REE), accelerometry to measure physical activity, and three 24-h diet recalls to measure energy intake.RESULTSMaternal glucose concentration during pregnancy was positively associated with children’s lean mass (P < 0.05) and adiposity (fat mass adjusted for lean mass; P < 0.05). The association between maternal glucose and children’s adiposity was independent of children’s REE, percent of time spent physically active, and energy intake (P < 0.001).CONCLUSIONSIntrauterine exposure to relatively high maternal glucose is associated with greater lean mass and adiposity among prepubertal offspring. Further research is needed to examine the mechanisms by which maternal glucose concentrations during pregnancy influence children’s body composition.