OBJECTIVE -Low birth weight (LBW), no early catch-up weight, and subsequent fat accumulation have been associated with increased risks of insulin resistance from childhood onward and later cardiovascular disease. We sought to clarify the effects of high birth weight (HBW) and postnatal weight gain on insulin resistance. RESEARCH DESIGN AND METHODS-A total of 117 obese children aged 10.4 Ϯ 2.4 years were divided into three groups according to fetal growth after exclusion of maternal diabetes. They were comparable for age, sex, puberty, and percent body fat. Customized French birth weight standards, adjusted for maternal characteristics and gestation number, identified subjects with true altered fetal growth: 32 had increased fetal growth according to customized standards (HBWcust), 52 were eutrophic, and 33 had restricted fetal growth according to customized standards (LBWcust). Fat distribution by dual-energy X-ray absorptiometry, insulin sensitivity indexes from an oral glucose tolerance test (OGTT), and leptin, adiponectin, and visfatin levels were compared between groups.RESULTS -The HBWcust subjects had a higher adiponectin level, higher whole-body insulin sensitivity index (WBISI), and lower hepatic insulin resistance index, lower insulin and free fatty acid concentrations during OGTT, and lower trunk fat percent than eutrophic (P Ͻ 0.05) and LBWcust subjects (P Ͻ 0.05). Besides birth weight, weight gain between 0 and 2 years was a positive predictor (P Ͻ 0.05) of WBISI, whereas weight gain after 4 years was a negative predictor (P Ͻ 0.05).CONCLUSIONS -HBW and early weight gain may program insulin sensitivity and adipose tissue metabolism and contribute to so-called metabolically healthy obesity. Diabetes Care 31:1031-1036, 2008N umerous studies have shown that low birth weight (LBW) is associated with an increased risk of insulin resistance, trunk accumulation of fat, metabolic syndrome, and cardiovascular disease in adulthood (1-3). Insulin resistance and metabolic syndrome have also been detected in children, adolescents, and young adults born small for gestational age (4 -6). Notably, the effect of birth weight on insulin resistance and later cardiovascular disease has been most apparent in the upper tertile of normal BMI and in obese subjects (7). In addition, the absence of early catch-up weight gain in the context of LBW has been shown to be the most deleterious (1,8).At the opposite extreme, the effect of high birth weight (HBW) on later insulin resistance and cardiovascular disease is more controversial. Some studies showed that subjects with HBW had lower rates of coronary heart disease and type 2 diabetes (2,9), whereas others reported that, in a context of gestational diabetes or in specific ethnic groups, the heaviest born babies also had an increased risk for developing obesity (10,11) and metabolic syndrome (12). This suggests that disease associations with higher birth weight may reflect the influence of maternal diabetes in both promoting larger birth size and conferring risk for diabetes t...
The three adenine nucleotide translocator (ANT1 to ANT3) isoforms, differentially expressed in human cells, play a crucial role in cell bioenergetics by catalyzing ADP and ATP exchange across the mitochondrial inner membrane. In contrast to differentiated tissue cells, transformed cells, and their rho(0) derivatives, i.e. cells deprived of mitochondrial DNA, sustain a high rate of glycolysis. We compared the expression pattern of ANT isoforms in several transformed human cell lines at different stages of the cell cycle. The level of ANT2 expression and glycolytic ATP production in these cell lines were in keeping with their metabolic background and their state of differentiation. The sensitivity of the mitochondrial inner membrane potential (Deltapsi) to several inhibitors of glycolysis and oxidative phosphorylation confirmed this relationship. We propose a new model for ATP uptake in cancer cells implicating the ANT2 isoform, in conjunction with hexokinase II and the beta subunit of mitochondrial ATP synthase, in the Deltapsi maintenance and in the aggressiveness of cancer cells.
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