The Effect of Obesity and Cushing's Disease on the Incorporation of Glucose into Lipid and Esterification of Palmitate by Human Adipose Tissue

Abstract

1. Rates of lipogenesis from glucose and palmitate have been measured in adipose tissue obtained from patients with obesity, diabetes, Cushing's disease and surgical controls. 2. Conversion of glucose into neutral lipid when expressed on the basis of tissue protein decreased in the following order: Cushing's patients, controls, obese patients. 3. A similar pattern of incorporation of T‐palmitate into neutral lipid was observed for the three groups of patients, except the differences were less marked. 4. Maximal activities of phosphofructokinase in adipose tissue are reduced in obesity (p< 0.05) and diabetics (p< 0.1) compared to surgical controls. 5. Five of the patients with Cushing's disease had an abnormal glucose tolerance test and showed a reduction in maximal activities of hexokinase (p< 0.05) in adipose tissue compared to the other four patients with Cushing's disease when expressed on a wet weight basis.

Chronic glucocorticoid treatment enhances lipogenic activity in visceral adipocytes of male Wistar rats

“…Studies specifically designed to explore the effects of GC on lipogenesis in WAT, performed in humans, rats or in adipose cell culture, are not so numerous and many of them gave conflicting results that left this issue still unanswered (Wilson & Galton , Bouillon & Berdanier , Campbell et al . , Gathercole et al .…”

Circulating Factors Affect 6-Phosphofructokinase Activity in Human Adipose Tissue

“…PFK activity in ovese subjects on weight-maintaining diets was signif icantly lower than in nonobese subjects on the same diet and was also lower than in the same obese subject on the reducing diet (p < 0.02). similar in adipose tissue obtained from obese and nonobese subjects during weight-mainte nance diet [4; Timmers and Knittle, unpub lished data], while rates of incorporation into triglyceride glycerol are the same [4] or lower in obese subjects [13], The lower activity of PFK in extracts of obese adipose tissue at weight maintenance [13] may be related to the decreased flux to triglyceride glycerol un der basal, in vitro conditions. However, the increased PFK activity in obese adipose tis sue during short periods of partial caloric restriction ( fig.…”

“…We hypothesized that the regulation of total tissue content of PFK activity might be related (if indirectly) to variations in glycolytic flux in adipose tis sue and/or to insulin sensitivity in vivo. Wil son and Galton have reported previously that PFK activity is lower in adipose tissue of obese nondiabetics [13] or obese diabetics [14,15] as compared to nonobese control subjects, and is restored to normal after treat ment of the same diabetics with insulin or oral agents [14]. We have studied insulinresistant obese subjects and nonobese con trols on isocaloric as compared to hypocaloric diets; the latter treatment would be expected to cause the disappearance of a pu tative factor causing impaired insulin sensi tivity in obese subjects at their maximum weight.…”