Accelerated Triglyceride Secretion A METABOLIC CONSEQUENCE OF OBESITY

Abstract

A new animal model was developed to determine the effect of obesity upon endogenous triglyceride secretion. Desert sand rats (Psammomys obesus), rodents which become spontaneously obese and hyperinsulinemic when given ad lib. chow, were given intravenous Triton to allow in vivo measurement of triglyceride secretion rates (TGSR). In a group of 18 fasted animals of varying body weight and degrees of obesity, TGSR correlated significantly with body weight (r = 0.68, P < 0.01) indicating that obesity was associated with accelerated endogenous release of triglyceride. In these same animals, basal plasma insulin levels correlated significantly with body weight (r = 0.78, P < 0.001) and TGSR correlated significantly with mean plasma insulin levels (r = 0.73, P <0.001), suggesting that hyperinsulinemia may have been the mechanism through which obesity enhanced TGSR. No correlation was found between basal triglyceride level and either body weight, basal insulin, or TGSR which suggested that individual triglyceride removal rates among the animals may have been variable. To test this hypothesis, seven animals were studied prospectively before and after induction of obesity. There were significant increases (P < 0.02) in all parameters, i.e., weight, plasma insulin level, TGSR, and basal triglyceride level. Thus, when each animal was used as its own control, thereby minimizing the postulated factor of variable individual triglyceride removal, increments in basal triglyceride were shown to accompany the development of obesity, hyperinsulinemia, and accelerated triglyceride secretion.These data from studies in the sand rat offer in vivo evidence that obesity leads to accelerated triglyceride

Transport of Very Low Density Lipoprotein Triglycerides in Varying Degrees of Obesity and Hypertriglyceridemia

“…This overproduction is consistent with results of several prior studies in both man and animals (28)(29)(30)(31). However, the importance of obesity as a cause of increased VLDL-TG flux may have been overlooked because of the method used for expressing results (32).…”

Determinants of human adipose tissue lipoprotein lipase. Effect of diabetes and obesity on basal- and diet-induced activity.

“…Thus, on the basis of the present study, apart from stressing adipose tissue participation, one cannot evaluate quantitatively the degree of defective TG removal in diabetic humans. The present results do not exclude the contribution of increased splanchnic TG production to the development of hypertriglyceridemia in diabetes, especially in those who were obese or had a familial form of hypertriglyceridemia (47)(48)(49). Thus, patient selection would be a major factor influencing the interpretation of the mechanism of hypertriglyceridemia in diabetes.…”

“…If so, the plasma TG removal capacity, as related to adipose tissue, would appear to be increased in obesity. There is evidence from animal studies indicating that obesity is accompanied by increased splanchnic TG production (47), which when coupled with increased removal, may explain the mild elevation of plasma TG associated with obesity. …”

Dietary fiber and lipoprotein metabolism in the genetically obese Zucker rat.

“…After 21 days of the experimental diet, triglyceride secretion rates (TGSR) were determined in animals which had fasted for 24 hours using the method of Triton hepatic blockade described by Robertson et al 14 and previously reported from this laboratory. 15 The Triton blockade of peripheral triglyceride removal results in a rise in plasma TG levels, reflecting TG secretion into the plasma.…”