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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male and female virgin rats and breeder rats with naturally-occurring diabetes, hypertension and arteriosclerosis, were made severely diabetic with a single, subcutaneous injection of alloxan (10 mg/100 g b.w.), after an 18 h fast. During five months of unrelenting diabetes, some animals became obese while others became emaciated. Only the emaciated animals survived but they were blind, their adrenal glands were hemorrhagic, hypertrophied and thrombosed, thymi involuted, kidneys swollen, hearts reduced in size while testes and ovaries were atrophic. Serum CPK, SGOT and SGPT were elevated concomitant with extensive cardiovascular damage, hepatic steatosis and generalized catabolism. Circulating triglycerides and free fatty acids were markedly elevated with total cholesterol only slightly increased. BUN and serum calcium levels were also greatly elevated. Sub-normal Cmpd. B levels indicated impaired adrenal steroidogenesis. Virgin rats developed arteriosclerosis and male and female breeder rats showed exacerbation of their pre-existing aortic sclerosis as well as P.A.N. lesions in their small-sized arteries. It is believed that severe diabetes causes exacerbation of the endogenous hormonal milieu resulting from abnormal hypothalamic-pituitary-adrenal function induced by repeated breeding, which conditions the connective tissue components of the arterial wall of rats toward accelerated degenerative changes.
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PMID:Polyarteritis nodosa induced in arteriosclerotic, male and female breeder rats by chronic alloxan diabetes. 1 32

Sexually mature, male and female Sprague-Dawley rats were housed in large communal breeding cages or in smaller paired breeding cages. Virgin control rats of the same age were housed similarly but segregated by sex. Breeders became obese, developed a fatty liver, and showed elevated levels of triglycerides, free fatty acids, and cholesterol. Breeders had high blood pressure, enlarged hearts, hyperglycemia, and islet beta cell degranulation. Serum enzymes, creatine phosphokinase, serum glutamic oxalo-pyruvic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, and blood urea nitrogen levels were elevated in breeder rats. The adrenal glands of male breeders appeared hyperactive; the adrenal glands of female breeders were thrombosed and appeared to be hypoactive. Male breeder rats developed microscopic aortic lesions only; female breeders developed advanced calcific aortic sclerosis. Male breeders kept in active stud service manifested the most abnormal metabolic and pathophysiological changes. Female breeders developed similar pathophysiological changes after four pregnancies, irrespective of their paired or communal breeding environment. Virgin rats were normal regardless of housing conditions. Our findings suggest that repeated breeding in male and female rats causes resetting of the hypothalamic-pituitary-adrenal-gonadal axis. This may lead to disturbed hormonal and metabolic changes which culminate with the development of accelerated cardiovascular degenerative changes.
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PMID:Pathophysiological differences between paired and communal breeding of male and female Sprague-Dawley rats. 33 92

A sub-strain of male and female spontaneously hypertensive rats (SHR) capable of having massively obese or non-obese offspring were bred repeatedly or were maintained as virgin controls. When the male and female breeders had sired or given birth to 5 litters of young, they were autopsied along with their 10-month-old celibate brothers and sisters. Virgin and breeder SHR developed high blood pressure (250 +/- 10 mm Hg). Breeder rats were significantly heavier than their virgin cohorts; pituitary and adrenal glands, hearts, and kidneys were significantly enlarged while thymi were severely involuted in breeder vs virgin SHR. The hyperlipidemia, fatty liver, hyperglycemia, and islet hyperplasia, characteristic of virgin SHR, were greatly exacerbated in breeder SHR. Blood levels of corticosterone, deoxycorticosterone, and aldosterone were greatly elevated in breeder vs virgin SHR. Although breeder rats of genetically normotensive strains develop aortic sclerosis, none of the breeder SHR developed aortic sclerosis. Instead, intimal fibrinohyalin lesions appeared confined to the testes and ovaries. It is suggested that the anatomical appearance or resistance of the arterial wall to the development of lesions is genetically mediated but this genetic programming may be modified by metabolic and hormonal factors with particular emphasis on the participation of adrenocorticoids.
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PMID:Hyperlipidemia, hyperglycemia and hypertension in repeatedly bred parents of the obese spontaneously hypertensive rat (obese/SHR) unaccompanied by arteriosclerosis. 674 80