Nutrition-Induced Variations in Responsiveness to Insulin Effects on Lipoprotein Lipase Activity in Isolated Rat Fat Cells

Abstract

The effect of insulin on the regulation of lipoprotein lipase (LPL) activity in isolated adipocytes from rats in various nutritional states was studied. Because LPL is secreted from adipocytes, possible insulin effects on LPL activity were assessed as 1) total cellular LPL activity, 2) LPL activity spontaneously secreted during incubations and 3) LPL secretion during perifusion of adipocytes preincubated with or without insulin. Incubation with insulin for 2 h produced no increase in LPL activity associated with adipocytes isolated from 5- to 6-wk-old fasted rats but increased by 83% the activity of LPL secreted into the incubation medium. Insulin pretreatment increased by 230% the capacity of the cells to secrete LPL activity when perifused in the presence of 5% fasted human serum. In adipocytes from young rats killed in the fed state, preincubation with insulin caused a small increase in cell-associated LPL activity (+21%) but no increase in LPL activity spontaneously secreted into the incubation medium. Similar to results in fasted rats, insulin-pretreated cells showed a 101% increase in their ability to secrete LPL activity during a perifusion. In contrast, larger adipocytes from 3-mo-old rats were totally unresponsive to insulin effects on both cellular and secreted LPL. However, 3 d of fasting followed by 9 d of refeeding restored responsiveness to insulin effects on both cellular and secreted LPL activity. Thus, variations in cellular responsiveness to insulin effects on LPL activity may play an important role in regulating nutrition-induced changes in LPL activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic and postprandial responses of plasma insulin, glucose and lipids in volunteers given dietary fibre supplements

“…A wave-like daily pattern in plasma TAG concentration is associated with highest values for adipose tissue LPL activity at 16.30 and 21.30 hours, and low values at 08.30 hours (Mirani-Oostdijk et al 1983). Low values at this time are consistent with a depressed adipose-tissue LPL response to insulin following a short fast (Fried et al 1990). As this response modulates CETP function it may explain, (1) the short duration of the TAG and HDL-cholesterol responses to lunch relative to those at breakfast in Expt 1, (2) the extended duration of the TAG response to a meal containing 47 g fat at 09.00 hours (D. L. Frape & A. M. Jones, unpublished results), compared with the response to a meal containing 87 g fat in Expt 1 given at 13.00 hours, and (3) the maintenance of HDLcholesterol concentration following chronic fibre supplementation and a glucose dose at 09.00 hours in Expt 2.…”

“…1 . 1 .34, LPL) secretion (Fried et al 1990). Adipose-tissue LPL activity modulates plasma concentrations of HDL-cholesterol (Eisenberg et al 1984) and probably of HDL,cholesterol (Taskinen & Nikkila, 1981) by influencing PP plasma TAG concentration (Tall, 1986 a).…”

Refeeding meal-fed rats increases lipoprotein lipase activity and deposition of dietary [14C]lipid in white adipose tissue and decreases oxidation to 14CO2. The role of undernutrition

“…It is generally assumed that plasma insulin is a key regulator of lipoprotein lipase activity in adipose tissue and that these are positively correlated (Cryer et al, 1976), but this was not apparent in the present experiments. However, there is evidence that the sensitivity of lipoprotein lipase to insulin may vary with nutritional state and adiposity (Fried et al, 1990) and may be influenced by levels of other circulating hormones (e.g. glucagon, adrenaline).…”

Stimulation of lipoprotein lipase synthesis by refeeding, insulin and dexamethasone

“…While this work was in progress, a series of papers have been published on the regulation by insulin or dexamethasone of lipoprotein lipase in human and rat adipose tissue and adipocytes [27][28][29][30][31][32]. Fried et al [27] found that in adipocytes of obese Zucker rats insulin stimulated lipoprotein lipase synthesis as a result of a general increase in protein synthesis.…”