Responsiveness to lipolytic agents and glycerol output from rat adipocytes is altered by the diabetic process. We have confirmed reports that preincubation is required for growth hormone-induced lipolysis in isolated fat cells. Isolated fat cells were prepared from the epididymal fat pads of normal and spontaneously diabetic BB Wistar rats (weight, 250-400 gm) and their nondiabetic littermates by collagenase digestion. Lipolysis was measured by glycerol release after sequential perifusion with buffer alone, bovine growth hormone 1 μg/ml, buffer alone, and epinephrine, 0.5 μmol/L in each case isolated fat cells from control, nondiabetic, and spontaneously diabetic rats were perifused under two conditions, with and without preincubation with bovine growth hormone. Isolated fat cells from control and nondiabetic rats did not respond to bovine growth hormone without preincubation. When preincubated with bovine growth hormone, response in control rats increased from nonpreincubated glycerol values of 4.9 to 13.5 nmol glycerol released/106 cells/min. In contrast to controls, nonpreincubated isolated fat cells from spontaneously diabetic rats that were stimulated with 1 μg/ml bovine growth hormone went from 18.0 to 42.6 nmol of glycerol released/106 cells/min. No preincubation was necessary in spontaneously diabetic rats. In addition, in all situations in which preincubation or the diabetic state enhanced lipolysis with growth hormone, similar enhancement was seen with epinephrine. For nondiabetic rats both preincubated and nonpreincubated isolated fat cells respond minimally to bovine growth hormone. In conclusion, preincubation with bovine growth hormone is not required to elicit lipolysis in perifused isolated fat cells from spontaneously diabetic BB rats. These data are comparable to data in the streptozotocin-diabetic rats and suggest that the diabetic process itself or the absence of insulin promotes responsiveness to growth hormone and upregulation of the growth hormone receptor. Furthermore, the enhanced responsiveness to growth hormone supports the idea that excess growth hormone is pathophysiologically active in the diabetes of the BB rat, possibly at both receptor and postreceptor levels.
|Original language||English (US)|
|Number of pages||7|
|Journal||The Journal of Laboratory and Clinical Medicine|
|State||Published - Jul 1991|