Lipid-Glucose Metabolism in Case with Markedly Reduced, Normally Functioning Adipose Tissue Mass

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In obesity, abnormal lipid and glucose metabolism, such as an increase in FFA and TG, abnormal GTT and hyperinsulinemia, has been well recognized. However, the mechanism by which such abnormalities in lipid and glucose metabolism occur is still unsolved. Salans et al. presented some evidence suggesting the cause of such metabolic abnormalities to be found in adipose tissue cell itself. When the cells were filled with fat, they became insulin-resistant which in turn reflected "insulin resistance" in obesity as a whole. The results obtained by these authors led us to a new idea to understand obesity to be "reduction of functioning adipose tissue mass", If so, we may expect a similar metabolic disturbance to that in obesity also in a case with anatomically reduced adipose tissue mass. From this point of view, metabolic studies were performed in total lipodystrophy and active Weber-Christian's disease in which adipose tissue mass is presumed to be anatomically reduced. In total lipodystrophy, an increase in FFA and TG, and hyperglycemia were observed. IRI and GH were normal, while ILA was extremely high. ILA was 15-32 times higher than the normal value in fasting serum. GTT was abnormal. On oral administration of glucose (50g), FFA decreased only slightly. However, IRI response seemed to be almost normal. There was no definite correlation between fasting FFA level and either IRI, GH or TG level. Intravenously injected 131I-insulin disappeared from circulation slightly slower in this case than in the control. Venous blood glucose, IRI and FFA responded very well to oral tolbutamide test. Capillary-venous glucose difference was also increased, suggesting an increase in uptake of glucose in peripheral tissues. An increase in FFA and TG was marked when the patient was given a high fat diet, in comparison with the period when she had been given a high carbohydrate diet. In the former period, serum lipoprotein pattern was "type V", while it was "type IV" in the latter. Post-heparin plasma LPL activity was almost normal. These results suggest that the increase in FFA on a regular or high fat diet in this patient may be at least partly due to the mechanism of "recycling of lipoprotein TG through FFA " at the acting sites of LPL. No increase in FFA was proved in in vitro incubation test, which suggests no intravascular lipolysis. Daily oral administration of Inderal decreased FFA, while noradrenaline infusion caused no appreciable increase in FFA and free glycerol. FFA-free glycerol ratio remained almost unchanged. In active Weber-Christian's disease, one patient (F. H.) was hyperlipemic and the other (N. S.) non-hyperlipemic. In case of hyperlipemic Weber-Christian's disease, an increase in FFA, TG, total cholesterol and total phospholipid was observed as in total lipodystrophy; but blood glucose level and GTT were normal. Marked hyperinsulinemia (IRI) was noticed. However, capillary-venous glucose difference was small. GH was normal. FFA decreased on oral glucose administration, and FFA-free glycerol ratio decreased only slightly, although free glycerol leve remained almost unchanged, which suggests an only slight increase in re-esterification of fatty acid in adipose tissue. There was neither definite correlation between fasting FFA level nor IRI, GH nor TG level. Serum lipoprotein pattern was "type IV". Intravenously injected 131I-insulin disappearance was slightly delayed. Post-heparin plasma LPL activity was markedly low. FFA decreased by daily oral administration of Inderal but did not increased by noradrenalin infusion.
Japan Society of Clinical Chemistryの論文

Lipid-Glucose Metabolism in Case with Markedly Reduced, Normally Functioning Adipose Tissue Mass

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