THE EFFECT OF INCREASED APPETITE AND OF INSULIN ON GROWTH IN THE HYPOPHYSECTOMIZED RAT

1958 ◽  
Vol 17 (2) ◽  
pp. 161-166 ◽  
Author(s):  
G. C. KENNEDY ◽  
DELPHINE M. V. PARROTT
Keyword(s):  
Normal Growth ◽  
Liver Cells ◽  
Regeneration Of The Liver ◽  
Hypothalamic Lesions ◽  
Protamine Insulin ◽  
Hypophysectomized Rats

SUMMARY Young hypophysectomized rats were subjected to hypothalamic lesions to increase their appetite. They became as fat as non-hypophysectomized rats treated in the same way, but unlike them retained appreciable amounts of extra protein and water. There was no growth in length, however, and the injection of zinc protamine insulin produced no additional effect either on growth or on appetite. During hyperphagia the greatest accumulation of protein was in the liver, and both the number and size of the liver cells increased. The weight of the kidney was much less affected. Neither normal growth nor regeneration of the liver appeared to be dependent, like that of the kidney or skeleton, upon the presence of the pituitary.

Effect of nutrition on growth and somatomedin A levels in the rat

1980 ◽  
Vol 94 (3) ◽  
pp. 321-326 ◽  
Author(s):  
Kazue Takano ◽  
Naomi Hizuka ◽  
Kazuo Shizume ◽  
Yoko Hasumi ◽  
Toshio Tsushima
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Normal Growth ◽  
Protein Diet ◽  
Low Protein Diet ◽  
High Fat ◽  
Low Protein ◽  
High Fat Diets ◽  
Hypophysectomized Rats ◽  
Fat Diets

Abstract. Serum somatomedin A was significantly reduced after 3 days of fasting in rats with a mean decrease of 23.6 ± 2.4% (N = 18) of initial values. Re-feeding for one day produced a definite increase in somatomedin A, with a rise in body weight. When re-fed isocalorically for 21 days with diets of different quality, a low protein diet led to smaller increases in both seum somatomedin A and body weight in comparison to those of control-, high-protein- and high fat-diets (P < 0.001). There is a positive correlation between the increase in body weight and serum somatomedin A levels (N = 70, r = 0.71, P< 0.001). The effect of growth hormone on somatomedin generation was abolished in hypophysectomized rats fed with low-protein diet. Our study suggests that protein in the diet is important for the generation of somatomedin A, which is necessary for normal growth.

Secretion of corticosterone in rats with anterior hypothalamic lesions

1963 ◽  
Vol 204 (4) ◽  
pp. 715-718 ◽  
Author(s):  
John C. Porter
Keyword(s):  
Intravenous Injection ◽  
Arginine Vasopressin ◽  
Hypothalamic Lesions ◽  
Hypophysectomized Rats ◽  
Collection Period ◽  
Low Rate

Secretory rates of corticosterone were determined in rats with intact hypothalami, in animals with anterior hypothalamic lesions, and in hypophysectomized rats with anterior hypothalamic lesions. Animals with intact hypothalami secreted 10.7, 13.2, 14.2, 14.7, 16.6, 17.5, 17.8, and 17.7 µg corticosterone in the first through the eighth 15-min interval, respectively, of a 2-hr collection period. Rats with hypothalamic lesions secreted 1.8, 2.7, 3.6, 6.1, 9.0, 10.7, 11.1, and 10.6 µg corticosterone in the first through the eighth 15-min interval, respectively. Intravenous injection of 100 mU arginine vasopressin every 30 min did not affect the rate of production of steroid in animals with lesions. Removal of the pituitary from rats with hypothalamic lesions reduced the secretion to 0.3 µg corticosterone in 15 min. Administration of 5 mU ACTH at half-hour intervals to animals with lesions greatly increased the rate of production of corticosterone, suggesting that the low rate during the first 15-min collection period was not due to an unresponsive adrenal. The magnitude of the response of the acutely hypophysectomized rats to ACTH was slightly less than that of animals with lesions.

Production of diabetes insipidus in hypophysectomized rats by hypothalamic lesions

1961 ◽  
Vol 201 (5) ◽  
pp. 811-814 ◽  
Author(s):  
C. C. Gale ◽  
S. Taleisnik ◽  
S. M. McCann
Keyword(s):  
Diabetes Insipidus ◽  
Water Intake ◽  
Median Eminence ◽  
Urine Volume ◽  
Water Turnover ◽  
Hypothalamic Lesions ◽  
Significant Augmentation ◽  
Hypophysectomized Rats ◽  
Somatotrophic Hormone ◽  
Made In

Lesions in the median eminence produced permanent diabetes insipidus (DI) in chronically hypophysectomized rats. Water turnover in these animals, however, was only about half of that observed when lesions were made in rats with intact pituitaries and was further characterized by absence of the normal interphase. Conversely, when hypophysectomy was performed in rats with DI, an immediate and sustained 50% reduction in water intake occurred. Administration of adrenocorticotropin to hypophysectomized rats with lesions caused significant augmentation of DI, but not to levels found in rats with DI and intact pituitaries. Neither somatotrophic hormone (STH) nor triiodothyronine increased water turnover when given to hypophysectomized animals with DI. Lesions in the median eminence of hypophysectomized rats induced an immediate increase in urine volume in the absence of water intake, which indicates that primary polyuria was responsible at least in part for the development of DI in hypophysectomized rats with lesions.

Growth hormone acutely increases glucose output by hepatocytes isolated from hypophysectomized rats

1989 ◽  
Vol 122 (2) ◽  
pp. 457-464 ◽  
Author(s):  
W. L. Blake ◽  
S. D. Clarke
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Liver Cells ◽  
Maximal Response ◽  
Isolated Rat Hepatocytes ◽  
Rat Liver Cells ◽  
Hypophysectomized Rats ◽  
Glucose Output

ABSTRACT A series of experiments using isolated rat hepatocytes was carried out to establish rat liver cells in suspension as a physiological model for examining GH responses, and to determine whether acute recombinant bovine GH (rbGH) treatment of rat liver cells increased glucose output and/or suppressed fatty acid synthesis from lactate. Rat liver cells were isolated by collagenase perfusion and incubated in short-term (<60 min) suspension. The amount of insulin, glucagon or vasopressin required to elicit a half-maximal response was within the physiological range of the circulating hormone. When hepatocytes from normal rats were acutely (<60 min) treated with 0, 0·1, 10, 100 or 1000 nmol rbGH/l, rates of hepatocyte glucose output and fatty acid synthesis were unaltered. In addition, acute rbGH treatment (1000 nmol/l) did not alter hepatocyte responsiveness to insulin or vasopressin. However, acute rbGH treatment of hepatocytes isolated from hypophysectomized rats significantly (P < 0·05) increased the rate of glucose output twofold and moderately (P<0·10) enhanced fatty acid synthesis. The accelerated rate of glucose production was not accompanied by an increase in the amount of glycogen phosphorylase-a. The observations with liver cells from hypophysectomized rats are not consistent with a GH receptor-transducing mechanism which is like that for glucagon (adenylate cyclase-linked) or insulin (tyrosine kinase-linked). Journal of Endocrinology (1989) 122, 457–464

HORMONAL BASIS FOR IMPAIRMENTS IN MILK SYNTHESIS AND MILK EJECTION FOLLOWING HYPOTHALAMIC LESIONS

1961 ◽  
Vol 23 (3) ◽  
pp. 303-316 ◽  
Author(s):  
C. C. GALE ◽  
S. TALEISNIK ◽  
H. M. FRIEDMAN ◽  
S. M. McCANN
Keyword(s):  
Median Eminence ◽  
Adrenal Glands ◽  
Regulatory Mechanisms ◽  
Adrenocorticotrophic Hormone ◽  
Milk Ejection ◽  
Hypothalamic Lesions ◽  
Severe Impairment ◽  
Electrolytic Lesions ◽  
Hypophysectomized Rats ◽  
Pituitary Secretion

SUMMARY The placing of electrolytic lesions in the median eminence of the hypothalamic tuber cinereum induces severe impairment of lactation in rats by causing deficiencies in pituitary secretion of adrenocorticotrophic hormone (ACTH; essential for milk synthesis) and of oxytocin (necessary for milk ejection). Thus, in rats with lesions given oxytocin × 2/day to permit milk ejection, it was observed that: (1) the severity of impairment in lactation correlated significantly with the degree of atrophy of the dams' adrenal glands; (2) administration of luteotrophin (LTH) failed to repair this defect in lactation; (3) when cortisol was administered milk production was markedly improved—to about 70–80% of normal for days 5–10—(a further slight increase in milk yield resulted when oxytocin injections were given every 4 hr. 'around the clock' to rats receiving cortisol therapy); and (4) administration of regimens consisting of either LTH and cortisol, or LTH, growth hormone (GH), and cortisol failed to improve lactation beyond levels attained with cortisol therapy alone. In hypophysectomized rats replacement with cortisol and LTH, plus oxytocin × 2/day, permitted substantial synthesis which was not significantly improved further when GH was added to the regimen, and which promptly declined when LTH therapy was withdrawn. Since no deficiency in secretion of LTH could be demonstrated in lactating rats with lesions given hormonal replacement, these data provide evidence that elimination of hypothalamic regulatory mechanisms by hypothalamic lesions is compatible with secretion of large amounts of LTH. This demonstration that lesions in the median eminence block release of ACTH while permitting continued secretion of LTH indicates that the hypothalamic mechanisms regulating their release are not identical.

The Morphology of Vacuolated Cells in the Liver Following Administration of Vitamin A.

1973 ◽  
Vol 31 ◽  
pp. 408-409
Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo ◽  
Fawzia Batti
Keyword(s):  
Electron Microscopy ◽  
Body Weight ◽  
Vitamin A ◽  
Light And Electron Microscopy ◽  
Liver Cells ◽  
Prominent Feature ◽  
Vascular Space ◽  
Vacuolated Cell ◽  
Vacuolated Cells ◽  
Vacuolated Cytoplasm

Vacuolated cells in the liver of young rats were studied by light and electron microscopy following the administration of vitamin A (200 units per gram of body weight). Their characteristics were compared with similar cells found in untreated animals.In rats given vitamin A, cells with vacuolated cytoplasm were a prominent feature. These cells were found mostly in a perisinusoidal location, although some appeared to be in between liver cells (Fig. 1). Electron microscopy confirmed their location in Disse's space adjacent to the sinusoid and in recesses between liver cells. Some appeared to be bordering the lumen of the sinusoid, but careful observation usually revealed a tenuous endothelial process separating the vacuolated cell from the vascular space. In appropriate sections, fenestrations in the thin endothelial processes were noted (Fig. 2, arrow).

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