We seek to determine if tissue-specific alterations in LPL are even more pronounced in the setting of NIDDM than in obesity. We hypothesize that subjects with NIDDM have a more pronounced defect in insulin-mediated glucose metabolism than obese subjects and have a greater increase in skeletal muscle LPL and that there is a continuum of SMLPL stimulation relative to insulin resistance in lean, obese and diabetic patients.
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