The histology and in vivo sulphate uptake of epiphyseal cartilage in protein-depleted rats

Shapiro, Brahm; Pimstone, B. L.

doi:10.1079/bjn19770117

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…Thus, GH levels could not be used in rats as an indicator of insufficient caloric intake. Administration of GH to malnourished patients and rats does not produce growth, because a GH resistance seems to occur (27). However, since GH replacement partially restored weight gain and tail length in our experiments it appears that the growth retardation was at least partly due to GH deficiency.…”

Section: Discussioncontrasting

confidence: 46%

Induction of reversible growth retardation and growth hormone deficiency by blockade of norepinephrine synthesis in the rat

Malozowski

Mamalaki²,

Pleti³

et al. 1993

Acta Endocrinologica

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Norepinephrine is a major regulator of the release of growth hormone. Diethyldithiocarbamate, a dopamine-\g=b\-hydroxylase inhibitor, reduces norepinephrine synthesis and acutely inhibits growth hormone (GH) secretion. To investigate the long-term effects of dopamine-\g=b\-hydroxylase blockade on growth, we administered diethyldithiocarbamate (0, 40, 100 or 400 mg/kg sc b.i.d.) to 21-day-old female rats for 10 days. Food intake, body weight, and tail length were measured twice a week. Plasma GH levels and hypothalamic dopamine and norepinephrine content were measured; messenger ribonucleic acids (mRNAs) for GH-releasing hormone and somatostatin were determined by quantitative in situ hybridization. Diethyldithiocarbamate administration decreased GH levels (p<0.05) and retarded growth in a dose-dependent manner (p<0.05), without altering food intake. Co-administration of GH partially reversed the growth retardation in diethyldithiocarbamate-treated animals (p<0.05). Diethyldithiocarbamate treatment also increased the hypothalamic dopamine/ norepinephrine ratio (1.13 vs 0.41 control, p<0.05). Local levels of GH-releasing hormone and somatostatin mRNA were not altered by treatment. After discontinuation of diethyldithiocarbamate, growth rates returned to normal or transiently even to supranormal values. Norepinephrine synthesis blockade with diethyldithiocarbamate provides a model for reversible growth retardation, in which GH levels are decreased in the absence of decreased GH-releasing hormone mRNA. These results support a role for norepinephrine in the regulation of normal growth. Saul Malozowski, Food and Drug Administration, 5600 Fishers Lane, HFD-510 Rockville, MD 20857, USA Growth hormone deficiency (GHD) is an important endocrine cause of short stature and can occur as a permanent or transient condition (1). After reversal of GHD or GH-resistant states, such as malnutrition, subjects resume normal growth velocity but the extent of accelerated "catch-up" growth varies.Three rodent models of GHD have been developed: hypophysectomy (2), neonatal administration of monosodium glutamate (MSG) (3-6) and the inbred dwarf mouse (7, 8). Hypophysectomy produces many other hormonal deficiencies besides GHD. Administration of toxic amino acids such as MSG results in abnormal behavior, such as tail self-mutilation; and there may be other hormonal abnormalities besides GHD. Colonies of inbred strains are difficult to obtain and to breed, and hormonal or metabolic alterations other than GHD also may cause growth retardation. All of these models have irreversible GHD. * This work was presented in part at the Endocrine Society Annual Meeting, Atlanta, 1990. Norepinephrine (NE) is an important regulator of GH secretion in the brain (9, 10). Exogenous administration of NE or other a-adrenergic agonists evokes GH secretion (11,12). Blockade of NE synthesis using the dopamine-/?-hydroxylase (DBH) inhibitor diethyldithiocarbamate (DDTC) (13, 14) has been studied widely as a means of acutely suppressing GH secretion. As DDTC ad...

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Section: Discussioncontrasting

confidence: 46%

Induction of reversible growth retardation and growth hormone deficiency by blockade of norepinephrine synthesis in the rat

Malozowski

Mamalaki²,

Pleti³

et al. 1993

Acta Endocrinologica

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“…The importance of IGF-1 in different nutritional states has been investigated mainly with respect to its serum concentrations. Shapiro & Pimstone (1977) first reported that G H could not stimulate growth in malnourished rats. This apparent GH resistance has been investigated using G H challenges.…”

Section: N U T R I T I O N a N D Igf-lmentioning

confidence: 99%

The Nutritional Regulation of Growth Hormone Action

Pell¹,

Bates

1990

Nutr. Res. Rev.

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is a single polypeptide chain of approximately 190 amino acids containing two intrachain disulphide bridges. It consists mainly of four anti-parallel a-helices which are differentiation. Later on, growth is clearly no longer a physiological priority for an animal, and GH is more concerned with the regulation of body composition. In ruminant animals, GH is also essential for mammary development and lactation; in primates, G H can influence lactational performance but it is the structurally related hormone, prolactin, which is most important (Cowie et al. 1980).

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Nutrition and somatomedin XVI: Somatomedins and somatomedin inhibitors in fasted and refed rats

1988

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The histology and in vivo sulphate uptake of epiphyseal cartilage in protein-depleted rats

Cited by 4 publications

References 28 publications

Induction of reversible growth retardation and growth hormone deficiency by blockade of norepinephrine synthesis in the rat

Induction of reversible growth retardation and growth hormone deficiency by blockade of norepinephrine synthesis in the rat

The Nutritional Regulation of Growth Hormone Action

Nutrition and somatomedin XVI: Somatomedins and somatomedin inhibitors in fasted and refed rats

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