Current Concepts of Somatomedin and Other Biologically Related Growth Factors

Chochinov, Ronald H.; Daughaday, William H.

doi:10.2337/diab.25.10.994

Cited by 75 publications

(12 citation statements)

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“…This increase in IRI was not mediated by changes in blood glucose concentration, and in view of its rapidity may represent a direct action of GH on insulin secretion since growth hormone intermediary hormones [20] may not be involved at this stage. Moreover, although glucagon has been shown to be released by GH even before insulin [21,22] and could therefore mediate GH-induced insulin release, the presence of high glucose levels abolishes GH-elicited glucagon release but amplifies the effect of GH on insulin release [21].…”

Section: Discussionmentioning

confidence: 87%

Effects of growth hormone on insulin release in the rat

Pierluissi

Ashcroft

1980

Diabetologia

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Summary. Growth hormone injected intravenously in the rat elicited a 6-fold spike change in immunoreactive insulin with little variation in glucose. Subcutaneous administration of growth hormone for 4 days augmented by 56% the insulin-secretory response to glucose of isolated islets from hypophysectomised rats but not the response of control rat islets. When islets were cultured in the presence of growth hormone, the glucose-induced insulin release was increased by 35 % in batch incubations of islets from both normal and hypophysectomised rats and by 70-110% in perifused islets. Thus the capacity for stimulated release of insulin is limited by hypophysectomy, and growth hormone is capable of directly influencing the secretory function of the/3-cell.

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Section: Discussionmentioning

confidence: 87%

Effects of growth hormone on insulin release in the rat

Pierluissi

Ashcroft

1980

Diabetologia

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“…As for the NSILA-S-carrier complex, its passage through blood capillaries seems also to be restricted as indicated by the absence of nonsuppressible insulin-like effects of circulating plasma in vivo. NSILA-S as well as either of its constituents, IGF I and IGF II, promote cell growth (1,5,20,31,32), stimulate sulfation of cartilage (5,33,34), and can be classified as somatomedins (35,36). In this context, the question will have to be examined next wvhether or not these effects, which are mediated via specific high affinity cell membrane receptors different from the insulin receptor (5,20,34), persist in the presence of the carrier protein.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the Action of Nonsuppressible Insulin-Like Activity on Isolated Rat Fat Cells by Binding to its Carrier Protein

Zapf¹,

Schoenle²,

Jagars³

et al. 1979

J. Clin. Invest.

177

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A B S T R A C T Nonsuppressible insulin-like activity extracted and purified from human serum (NSILA-S) mimics all insulin-like effects in vitro and, after injection, in vivo in the presence of excess insulin antibodies. However, there is no evidence that it exerts acute insulin-like effects in its native form in the circulation, where it is almost completely bound to a specific large molecular weight carrier protein. In this paper we show that partially purified NSILA-S-carrier protein, devoid ofendogenous insulin-like activity, inhibits the stimulatory effect of NSILA-S, but not of insulin, on 3-0-methylglucose transport and on lipogenesis from [U-14C]glucose in isolated rat fat cells. Concomitantly, it prevents binding of 125I-labeled NSILA-S to the insulin receptor and to the NSILA-Sbinding site.The following explanation is, therefore, offered for the absence of acute insulin-like effects of native NSILA-S in vivo: In native serum NSILA-S occurs alfmost exclusively as NSILA-S-carrier complex. Ac-cording to recent findings the passage of this complex through blood capillaries is restricted. The present results indicate that, in addition, it is metabolically inactive, or, at least, possesses reduced metabolic activity. The well-known phenomenon that whole serum, nevertheless, exerts pronounced nonsuppressible insulin-like effects on adipose tissue in vitro seems, therefore, to be mainly caused by the presence of a large molecular weight insulin-like protein not identical to the NSILA-S-carrier complex.

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“…[3H]thymidine incorporation into chondrocytes; Chochinov & Daughaday, 1976) or matrix production (evaluated by measurement of [35S]sulphate incorporation into matrix components, i.e. the so-called 'sulphation factor ';Dziewiatkowski, 1964;Daughaday, Hall, Raben, Salmon, Van den Brande & Van Wyk, 1972).…”

Section: Discussionmentioning

confidence: 99%

Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats.

Hunziker

Schenk

1989

The Journal of Physiology

279

310

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SUMMARY1. Chondrocyte activities within growth plate cartilage are the principal determinants of longitudinal bone growth, and it was the aim of this investigation to assess how these cell activities are modulated under various growth rate conditions.Using proximal tibial growth plates from rats of different ages, growth rate was determined by fluorochrome labelling and incident light fluorescence microscopy. Various cellular parameters contributing to longitudinal bone growth were quantified by light microscopic stereology. The size of the proliferating cell population ('growth fraction') was estimated by autoradiography (using [3H]thymidine labelling).2. A comparison between data for suckling (21-day-old) and fast-growing (35-dayold) rats revealed that growth acceleration is achieved almost exclusively by cellshape modelling, namely by an increase in final cell height and a decrease in lateral diameter, whereas final cell volume and surface area are slightly reduced. Cell proliferation rate in the longitudinal direction and net matrix production per cell remain unchanged. The physiological increase in linear growth rate thus appears to be based principally upon a controlled structural modulation of the chondrocyte phenotype. On the other hand, a physiological reduction in growth rate (i.e. growth deceleration) effected during the transition from pre-puberty (35-day-old rats) to maturity (80-day-old rats) is achieved by simultaneous decreases in several chondrocyte parameters, including cell height (i.e. phenotype modulation), cell volume and proliferation rate (in the longitudinal direction

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Current Concepts of Somatomedin and Other Biologically Related Growth Factors

Cited by 75 publications

References 0 publications

Effects of growth hormone on insulin release in the rat

Effects of growth hormone on insulin release in the rat

Inhibition of the Action of Nonsuppressible Insulin-Like Activity on Isolated Rat Fat Cells by Binding to its Carrier Protein

Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats.

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