Decrease in Serum Receptor-Reactive Somatomedin in Diabetes

Baxter, Robert C.; Brown, Allan H.; Turtle, John R.

doi:10.1055/s-0028-1092711

Cited by 31 publications

(22 citation statements)

References 6 publications

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“…In recent studies utilizing diabetic humans (WtNTER et al, 1980;BLETHEN et al, 1981), and streptozotocin-induced diabetic rats (PHILLIPS & YOUNG, 1976;BAXTER et al, 1979;MEAS et al, 1983), serum IGF-I levels are lowered by as much as 40-50% of control non-diabetics. These "end-point" studies, however, were not able to address whether or not changes in serum IGF-I levels occur prior to the onset of the disease.…”

Section: Discussionmentioning

confidence: 95%

“…IGF-I is a circulating polypeptide with growth promoting and metabolic properties similar to those of insulin (FRoESCH • ZAPH, 1985). In diabetic humans (WINTER et al, 1980;BLETHEN et al, 1981), who are in poor metabolic control and in rats with streptozotocin induced ketotic diabetes (PHILLIPS & YOUNG, 1976;BAXTER et al, 1979;MEAS et al, 1983;ROSSETTI et al, 1991), serum levels of IGF-I are lowered by as much as 40-50~ of control non-diabetics. Recent investigations have linked the decreased plasma levels of IGF-I to decreased expression of IGF-I mRNA (GOLDSTEIN et al, 1988;BORNFELDT et al, 1989;BONI-SCHNETZLER et al, 1989).…”

Section: Introductionmentioning

confidence: 96%

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Insulin-like growth factor I levels decrease in the development of diabetes inMacaca nigra

et al. 1995

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ABSTRACT. Members of the monkey species Macaca nigra spontaneously develop impairments in insulin secretion and glucose clearance, and eventually become overtly diabetic. Changes in certain metabolic signals such as clearance of glucose and insulin increment secreted in an intravenous glucose tolerance test have allowed the identification of four stages in the progression from nondiabetes to diabetes in monkeys --non-diabetic, hormonally impaired, borderline diabetic, and diabetic. Recently, another metabolic stage, hyperinsulinemic, was also identified in these animals. In recent years, other factors besides those listed above have been implicated to be correlated with the metabolic progression from a nondiabetic to a diabetic state. One of these factors, is insulin like growth factor I (IGF-I). In diabetic humans who are in poor metabolic control, and in rats with streptozotocin induced ketotic diabetes, serum levels of IGF-I are lowered by as much as 40-50~ of control non-diabetics. If indeed decreased IGF-I levels are correlated with the onset of diabetes then changes in IGF-I concentrations prior to the clinically diagnosed disease state would be expected.Using serum samples collected from different animals in a colony of Macaca nigra in a variety of metabolic states, we have found that IGF-I and insulin levels decrease in each defined metabolic state as the animals progress from nondiabetic to diabetic. Since IGF-I and insulin levels decrease in a similar fashion in the progression of this disease then this maybe indicative of the coordinate expression of these two factors.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 96%

Insulin-like growth factor I levels decrease in the development of diabetes inMacaca nigra

et al. 1995

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“…One regulatory factor known to affect both receptor types and SM-C/IGF-I is GH itself. GH secretion is decreased in both fasting [22] and diabetes [23], conditions where hepatic GH and PRL receptors, and serum SM-C/IGF-I levels [4,21,24], are diminished. Our results could be explained if an adrenal factor, perhaps a catecholamine, were found to be a physiological regulator of pituitary GH secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Insulin treatment restored these receptors to normal levels. The circulating level of the GH-dependent growth factor somatomedin-C (identical to insulin-like growth factor-I [3] and designated SM-C/IGF-I) also decreases in experimental diabetes [4]. It has been suggested that the loss of G H receptors might be associated with the decrease in SM-C/IGF-I, although there is some evidence that the growth factor and receptor levels fall at different rates [5].…”

mentioning

confidence: 99%

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

Bryson

Baxter

1986

Diabetologia

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Summary. Streptozotocin-induced diabetes causes a decrease in growth hormone and prolactin receptors in the livers of female rats, and in the serum concentration of somatomedin-C/ insulin-like growth factor-I, concomitantly with an increase in the serum testosterone levels. In this study, a possible role for adrenal androgens in the loss of receptors was examined. Rats were adrenalectomised bilaterally 3 days after the induction of diabetes with streptozotocin (100mg/kg intravenously), and livers were removed 3 days later. Adrenalectomy had no effect on binding of ovine prolactin or bovine growth hormone to liver microsomal membranes from non-diabetic rats, but in diabetic rats it entirely abolished the 56% decrease in prolactin binding and significantly reversed the 66% decrease in growth hormone binding and the parallel fall in serum levels of somatomedin-C/insulin-like growth factor-I (p<0.05). Adrenalectomy also prevented the diabetes-induced rise in serum testosterone. Daily injection of testosterone to normal and diabetic rats for 12 days significantly reduced both prolactin and growth hormone binding (p< 0.001), with the effect of diabetes being additive upon the testosterone effect. Implantation of testosterone-filled silastic capsules at the time of adrenalectomy (i. e. for 3 days) did not prevent the adrenalectomy-induced restoration of both growth hormone and prolactin receptors. The resulting high serum testosterone level did not reduce binding to growth hormone receptors in control rats over the 3 day period, and caused no further decrease in diabetic rats. However, binding to prolactin receptors was reduced by 47% in control animals with no further loss in diabetic animals (p < 0.001). Adrenalectomy prevented the loss of prolactin receptors in both testosterone-treated and diabetic rats. These results indicate that, whether or not the rise in testosterone of adrenal origin contributes to the receptor loss in diabetes, the effect also depends on another factor of adrenal origin.

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“…IGF-I mRNA content in diabetic liver was selectively reduced. The reduction in circulating IGF-I concentration in diabetic rats [31][32][33] is likely to be closely tied to the profound fall in liver IGF-I mRNA. It is estimated that the 31 ~g/day produced in liver could account for almost all of the circulating concentration of about 800 ng/ml [8,34].…”

Section: Discussionmentioning

confidence: 99%

Reduced insulin-like growth factor-I mRNA content in liver, adrenal glands and spinal cord of diabetic rats

1994

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Decrease in Serum Receptor-Reactive Somatomedin in Diabetes

Cited by 31 publications

References 6 publications

Insulin-like growth factor I levels decrease in the development of diabetes inMacaca nigra

Insulin-like growth factor I levels decrease in the development of diabetes inMacaca nigra

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

Reduced insulin-like growth factor-I mRNA content in liver, adrenal glands and spinal cord of diabetic rats

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