scholarly journals Immunohistochemical Studies of Early Changes of Pituitary Glands Induced by Synthetic Salmon Calcitonin(sCT) in Sprague-Dawley Rats. Experimental Models for the Human Alpha-Subunit-Producing Pituitary Adenomas.

1999 ◽  
Vol 32 (4) ◽  
pp. 345-350
Author(s):  
Masanori Murakoshi ◽  
Rie Ikeda ◽  
Toshi Horiuchi ◽  
Takaharu Nakayama ◽  
Reiko Kurotani ◽  
...  
1992 ◽  
Vol 42 (6) ◽  
pp. 401-407 ◽  
Author(s):  
R. Yoshiyuki Osamura ◽  
Masanori Murakoshi ◽  
Rie Inada ◽  
Toshi Horiuchi ◽  
Kei-ichi Watanabe

Author(s):  
D. J. McComb ◽  
J. Beri ◽  
F. Zak ◽  
K. Kovacs

Investigation of the spontaneous pituitary adenomas in rat have been limited mainly to light microscopic study. Furth et al. (1973) described them as chromophobic, secreting prolactin. Kovacs et al. (1977) in an ul trastructural investigation of adenomas of old female Long-Evans rats, found that they were composed of prolactin cells. Berkvens et al. (1980) using immunocytochemistry at the light microscopic level, demonstrated that some spontaneous tumors of old Wistar rats could contain GH, TSH or ACTH as well as PRL.


1988 ◽  
Vol 7 (5) ◽  
pp. 603-615 ◽  
Author(s):  
G.T. Gallagher ◽  
E.A. Maull ◽  
K. Kovacs ◽  
S. Szabo

Male Sprague-Dawley rats ingested 0, 20 ppm, or 500 ppm of acrylonitrile in drinking water for 2 years. Rats receiving 500 ppm of acrylonitrile exhibited early mortality and retarded weight gain. Tumors of Zymbal's gland were associated in dose-response fashion with acrylonitrile exposure. Age-associated incidence of pituitary adenomas containing immunoreactive prolactin was decreased in acrylonitrile-treated rats. A decrease in pituitary tumor incidence also was observed in rats treated with low doses of acrylonitrile, suggesting that reduction in this tumor frequency was not because of early death. No increases were found in tumors of other organ systems, but a trend toward development of forestomach papillomas was noted in rats receiving the highest concentration of acrylonitrile.


2007 ◽  
pp. 183-192
Author(s):  
š Mozeš ◽  
z Šefčíková ◽  
Ľ Lenhardt

To investigate the relationship between early nutritional experience, ontogeny of the small intestinal functions and predisposition to obesity development, the following experimental models of male Sprague-Dawley rats were used: 1) rats in which the quantity of nutrition was manipulated from birth to weaning (day 30) by adjusting the number of pups in the nest to 4 (SL), 10 (NL) and 16 pups (LL) and 2) littermates of SL, NL and LL rats fed either a standard or a hypercaloric diet from days 80 to 135 of age. The overfed SL pups were overweight after day 15 and became permanently obese, whereas the underfed smaller LL pups, due to accelerated growth and enhanced food intake from day 30 to day 35, attained a body fat level that did not differ from normally fed NL rats. Moreover, a significantly increased duodenal and jejunal alkaline phosphatase (AP) activity was found in SL and LL rats and these acquired somatic and intestinal characteristics persisted from weaning throughout life. Eight weeks of high-energy diet feeding elicited a similar pattern of intestinal response in SL and LL rats that was clearly different from NL rats. Despite energy over-consumption in these three groups, both SL and LL rats still displayed enhanced AP activity and showed a significant increase in protein/DNA ratio accompanied with a significant body fat accretion. These results indicate that the postnatally acquired small intestinal changes induced by over- and undernutrition could be involved in the similar predisposition to obesity risk in later life when caloric density of the diet is raised.


1974 ◽  
Vol 62 (2) ◽  
pp. 213-223 ◽  
Author(s):  
SAKAE KIKUYAMA ◽  
HIROSHI NAGASAWA ◽  
REIKO YANAI ◽  
KOREHITO YAMANOUCHI

SUMMARY Female Sprague—Dawley rats were fed 6-propyl-2-thiouracil (PTU) in their diet during late pregnancy and lactation. The growth and gonadal development of their pups were inhibited and in females the day of vaginal opening and onset of oestrous cycles were delayed; thyroid glands were hypertrophied. Treatment of the pups with thyroxine largely reversed these changes. The effect on body weight persisted even after treatment with PTU had stopped. At 20 days of age, the anterior pituitary glands of the pups of PTU-treated mothers contained significantly less growth hormone (GH) and prolactin than those of normal pups of both sexes. These changes persisted at 60 days of age. If the pups of PTU-treated mothers were given thyroxine from day 1 to day 20 of age, pituitary GH and prolactin content on day 20 had returned towards normal values. Thyroid deficiency was found to suppress the synthesis and release of prolactin and the synthesis of GH by the pituitary in vitro. These findings suggest that thyroxine influenced the maturation of the pituitary directly and/or through the hypothalamus and that thyroxine deficiency in early life brought about persistent alteration of the pituitary secretion of GH and prolactin.


2002 ◽  
Vol 30 (1) ◽  
pp. 28-40 ◽  
Author(s):  
Jun Zhang ◽  
Eugene H. Herman ◽  
Alan Knapton ◽  
Douglas P. Chadwick ◽  
Virgil E. Whitehurst ◽  
...  

2018 ◽  
Vol 314 (1) ◽  
pp. F81-F88 ◽  
Author(s):  
Debra L. Irsik ◽  
Jian-Kang Chen ◽  
Michael W. Brands

Hyperinsulinemia has been hypothesized to cause hypertension in obesity, type 2 diabetes, and metabolic syndrome through a renal mechanism. However, it has been challenging to isolate renal mechanisms in chronic experimental models due, in part, to technical difficulties. In this study, we tested the hypothesis that a renal mechanism underlies insulin hypertension. We developed a novel technique to permit continuous insulin infusion through the renal artery in conscious rats for 7 days. Mean arterial pressure increased by ~10 mmHg in rats that were infused intravenously (IV) with insulin and glucose. Renal artery doses were 20% of the intravenous doses and did not raise systemic insulin levels or cause differences in blood glucose. The increase in blood pressure was not different from the IV group. Mean arterial pressure did not change in vehicle-infused rats, and there were no differences in renal injury scoring due to the renal artery catheter. Glomerular filtration rate, plasma renin activity, and urinary sodium excretion did not differ between groups at baseline and did not change significantly with insulin infusion. Thus, by developing a novel approach for chronic, continuous renal artery insulin infusion, we provided new evidence that insulin causes hypertension in rats through actions initiated within the kidney.


2006 ◽  
Vol 291 (2) ◽  
pp. F384-F394 ◽  
Author(s):  
Inna Sinuani ◽  
Zhan Averbukh ◽  
Inna Gitelman ◽  
Micha J. Rapoport ◽  
Judit Sandbank ◽  
...  

The present study investigated the role of IL-10 produced by the mesangial cells in postnephrectomy compensatory renal growth and the effect of the immunomodulator AS101 on this process. One hundred forty unilateral nephrectomized and sham-operated male Sprague-Dawley rats were treated by AS101 or PBS before and after surgery. The results show that secretion of IL-10 and TGF-β by mesangial cells isolated from the remaining kidneys was increased significantly, compared with those of control and sham animals. Moreover, TGF-β secretion by mesangial cells was increased after the addition of exogenous recombinant IL-10 and inhibited in the presence of neutralizing anti-IL-10 antibodies. In vivo, compensatory growth of the remaining kidneys was associated with significant increase in IL-10 content in renal tissues and plasma. Immunohistochemical studies show that IL-10 was produced by mesangial cells. Elevated IL-10 levels were followed by the rise in TGF-β content in plasma and renal tissue. AS101 treatment decreased IL-10 and TGF-β expression in plasma and kidney tissues and results in 25% reduction in the fresh and fractional kidney weight and decreased hypertrophy of tubular cells (protein/DNA ratio, morphometric analysis). Taken together, these data demonstrate that TGF-β production by mesangial cells is IL-10 dependent. Mesangial cells are the major source of IL-10 in kidneys. AS101, by inhibiting the activity of IL-10, decreases TGF-β production by mesangial cells, thus limiting compensatory tubular cell hypertrophy.


2020 ◽  
Vol 22 (1) ◽  
pp. 360
Author(s):  
Ryan Fitzgerald ◽  
Andrew Olsen ◽  
Jessica Nguyen ◽  
Winifred Wong ◽  
Malek El Muayed ◽  
...  

Cadmium (Cd) is an anthropogenic as well as a naturally occurring toxicant associated with prediabetes and T2DM in humans and experimental models of Cd exposure. However, relatively few studies have examined the mechanism(s) of Cd-induced hyperglycemia. The purpose of this study was to examine the role of pancreatic islets in Cd-induced hyperglycemia. Male Sprague–Dawley rats were given daily subcutaneous doses of Cd at 0.6 mg/kg over 12 weeks. There was a resulting time-dependent increase in fasting blood glucose and altered insulin release in vitro. Islets isolated from control (saline-treated) and Cd-treated animals were incubated in low (0.5 mg/mL) or high (3 mg/mL) glucose conditions. Islets from 12 week Cd-treated animals had significantly less glucose-stimulated insulin release compared to islets from saline-treated control animals. The actual Cd content of isolated islets was 5 fold higher than the whole pancreas (endocrine + exocrine) and roughly 70% of that present in the renal cortex. Interestingly, islets isolated from Cd-treated animals and incubated in high glucose conditions contained significantly less Cd and zinc than those incubated in low glucose. These results show that within whole pancreatic tissue, Cd selectively accumulates in pancreatic islets and causes altered islet function that likely contributes to dysglycemia.


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