Key result
Higher BMI strongly correlates with declining hormone-stimulated skeletal muscle glucose transport up to ~30 kg/m2.
Why the study?
Does body mass index correlate with hormone-stimulated glucose transport in human skeletal muscle?
Cross-Sectional (n=30)
Does body mass index correlate with hormone-stimulated glucose transport in human skeletal muscle?
Effect estimate: R = 0.765
Insulin resistance in skeletal muscle shows a continuous decline with increasing BMI rather than a specific obesity threshold, with complete loss of hormone-stimulated glucose transport above a BMI of approximately 30 kg/m2.
Hypothesis-generating for continuous BMI-related muscle insulin resistance; prospective studies needed before clinical thresholds shift.
We have shown that maximally stimulated glucose transport is reduced in in vitro incubated muscle of morbidly obese subjects. To investigate the possibility that a "threshold" of obesity exists, above which glucose transport is significantly decreased, hormone (insulin, IGF-I, or IGF-II) stimulation of glucose transport was correlated with body mass index using muscle biopsies from a group of 30 lean to obese females with BMI ranging from 16 to 40. There was a significant negative relationship between stimulation for glucose transport and BMI (R = 0.765). These data suggest there is no obesity threshold for insulin resistance in skeletal muscle but a continuous decline in glucose transport below a BMI of approximately 30 kg/m2, after which insulin and the IGFs no longer stimulate glucose transport.
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Elton et al. (1994) conducted a cross-sectional in Obesity (n=30). Body mass index was evaluated on Hormone (insulin, IGF-I, or IGF-II) stimulation of glucose transport (R = 0.765). Body mass index had a significant negative correlation with hormone-stimulated glucose transport in skeletal muscle (R = 0.765), indicating a continuous decline up to a BMI of approximately 30 kg/m2.
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