Why the study?
Does a weight reduction program using supplemented fasting improve serum lipoproteins and lipoprotein lipase activity in poorly controlled, obese, Type II diabetics?
Does a weight reduction program using supplemented fasting improve serum lipoproteins and lipoprotein lipase activity in poorly controlled, obese, Type II diabetics?
Supplemented fasting in obese type II diabetics leads to sustained reductions in VLDL triglycerides and increases in HDL cholesterol, likely driven by reduced lipoprotein synthesis rather than increased clearance.
Supplemented fasting may improve lipids in obese type II diabetics; hypothesis-generating and requires randomized confirmation before practice change.
Poorly controlled, obese, Type II diabetics were studied before, during, and 3 months after a weight reduction program that used supplemented fasting (200 kcal or 0.9 MJ/day). During fasting, the very low density lipoprotein (VLDL) triglycerides (TG) decreased, as did the adipose tissue lipoprotein lipase (AT-LPLA) and skeletal muscle lipoprotein lipase (SM-LPLA) activities. Three months later VLDL TG remained low (-59%), while high density lipoprotein cholesterol was higher (+11%) and blood glucose control improved compared with values on admission. The fractional removal rate (K2) at the i.v. fat tolerance test (IVFTT) and the SM-LPLA were unchanged, while AT-LPLA (expressed per gram of wet weight, but not as whole-body AT-LPLA) increased by 25%. There were no significant correlations between AT-LPLA and the lipoprotein TG concentrations or K2-IVFTT, although there were significant positive correlations between SM-LPLA and K2-IVFtt, both on admission and after body weight stabilization. This may indicate that SM-LPLA is more directly related to the capacity to remove lipoprotein TG, at least in obese diabetic patients. K2-IVFTT was inversely correlated to the VLDL TG and cholesterol concentrations both before and 3 months after fasting. Because both SM-LPLA and K2-IVFTT were unchanged after body weight reduction, the change in VLDL TG may be mainly due to a reduced rate of lipoprotein synthesis.
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Vessby et al. (1985) studied this question.
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