The lack of impact of the R117H mutation on chloride secretion in intestine and nose contrasts with the ~80% loss of CFTR activity reported in patch clamp studies. Apparently CFTR activity is not rate-limiting for chloride secretion in both tissues at levels >20% of normal, or compensatory factors may operate that are absent in heterologous host cells in vitro.
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)
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