Growth and Obesity Following Ventromedial Hypothalamic Lesions Placed in Female Rats at Four Different Ages

Bernardis, Lee L.; Skelton, Floyd R.; Bahorsky, Michael; Bohacek, Luise

doi:10.1159/000121674

Cited by 74 publications

(15 citation statements)

References 9 publications

(16 reference statements)

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“…Kennedy postulated that hyperphagia could not appear in these rapidly growing young rats since they were already eating maximally. Han et al (1965) and Bernardis and Skelton (1965) confirmed these findings and the latter authors observed, in addition, a decrease in the number of pituitary acidophils in spite of an intact median eminence. Similar findings were then reported for the male weanling rat (Bernardis and Skelton, 1967) and extended by the observation (Bernardis and Frohman, 1967;Frohman and Bernardis, 1968) that plasma and pituitary growth hormone (GH) levels were decreased as measured by radioimmunoassay in the weanling rat with VMN lesions.…”

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confidence: 73%

Origin of endocrine‐metabolic changes in the weanling rat ventromedial syndrome

Bernardis

Goldman

1976

J of Neuroscience Research

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Destruction of the ventromedial hypothalamic nuclei (VMN) in the weanling rat without injury to the median eminence results in a series of somatic, endocrine, and metabolic changes that are characterized by normal food and water intake but decreased linear growth, normal body weight but increased carcass fat and reduced carcass protein, lean body mass, and water. The endocrine alterations comprise hyperinsulinemia in the face of normoglycemia, hypertriglyceridemia and hypercholesterolemia and reduced growth hormone levels. The metabolic changes include greater oxidation of glucose and incorporation into lipid and reduced palmitate oxidation but increased incorporation into lipid. Weanling rats with VMN lesions are normophagic in absolute terms, relative to body weight and per metabolic unit, but their nocturnal feeding and weight gain cycles are disrupted and their locomotor activity is reduced. The VMN are involved in the long-term control of feeding - as in the mature rat - as shown by intragastric preloading studies and dietary density manipulation, glucose preference tests and intraperitoneal injections with glucose. Hyperinsulinemia and hypertriglyceridemia are present four days after the VMN operation in the presence of subnormal food intake and plasma glucose levels. Manipulations of the fat content of the diet revealed that the hyperlipidemia is of both endogenous and exogenous origin and that lipoprotein lipase is increased; a 48-hour fast reduced the hyperlipidemia to control levels, however. This suggests that weanling VMN rat tissue may have an impaired ability to take up circulating lipid. An increased incorporation of glycerol into lipid may be due to induction of glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed neither depressed lipolysis nor diminished lipolytic activity per milligram of tissue protein. Glucose oxidation and incorporation into adipose tissue is increased in several tissues in vitro and there is enhanced glucose disappearance from plasma and incorporation into tissue lipids in vivo. These changes develop within a short time after lesion production and persist at least partially up to six months: glucose utilization in liver increases already four hours after the operation whereas it takes 72 hours to commence in adipose tissue. Insulin resistance is not apparent either in vivo or in vitro. The decreased growth hormone levels are not critical to the metabolic changes, nor is the hyperinsulinemia totally necessary. The metabolic changes also appear on several different types of diet and persist with fasting. The latter does not reduce insulin sensitivity of VMN rat tissues, wheras it does so in normal rats. Mature rats developed the same metabolic changes even in the absence of hyperphagia. The metabolic alterations can be blocked by pharmacologic doses of glucocorticoids, but are enhanced by the administration of estrogen...

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supporting

confidence: 73%

Origin of endocrine‐metabolic changes in the weanling rat ventromedial syndrome

Bernardis

Goldman

1976

J of Neuroscience Research

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“…No estimate of energy expenditure was undertaken in the present study and further detailed examination of the pattern of food intake in treated animals and of energy expenditure appear indicated. Han et al [18] and Bernardis & Skelton [19,20] have shown that weanling rats with electrolytic lesions in the ventromedial hypothalamic nuclei became obese without excessive caloric intake. Frohman and Bemardis [6] concluded that at least one major factor contributing to excessive accumulation of adipose tissue in VMN lesioned weanling rats was growth hormone deficiency resulthag from the hypothalamic lesions.…”

Section: Discussionmentioning

confidence: 99%

Effects of monosodium glutamate administration in the neonatal period on the diabetic syndrome in KK mice

1976

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Summary. Administration of monosodium glutamate (MSG) to KK mice during the neonatal period resulted in a syndrome of obesity, stunting and hypogonadism. In some animals the genetic predisposition to diabetes was unmasked with the development of marked hyperglycaemia and or hyperinsulinaemia. Food intake was not increased compared to controls. The elevated plasma glucose and insulin in fed MSG treated mice fell rapidly with food deprivation. Glucose disposal was comparable in MSG treated and control mice after IP glucose, but after oral glucose MSG treated mice showed impaired glucose tolerance. Insulin secretion was defective in MSG treated mice after IP but not after oral glucose.

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“…In contrast, linear growth (body length, tail length) was reduced most in Group 1, less in Groups 3 and 5, and was unaffected in Group 7. It was slightly less (10 %) in males than in females (15%, Bernardis & Skelton, 1966). It is possible that the greater effect of ventromedial lesions in weanling rats is attributable to a greater vulnerability of the smaller brains in these animals.…”

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confidence: 86%

“…

Male Holtzman rats received bilateral electrolytic lesions at the age of 26 days (Group 1), 59 days (Group 3), 75 days (Group 5) and 140 days (Group 7).

…”

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confidence: 92%

Growth and Obesity in Male Rats After Placement of Ventromedial Hypothalamic Lesions at Four Different Ages

Bernardis¹,

Skelton²

1967

Journal of Endocrinology

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Ventromedial hypothalamic lesions in weanling female rats have been reported to result in a greater reduction of growth than placement of such lesions in older animals (Bernardis & Skelton, 1966). The present report deals with a parallel study in male rats of corresponding ages.Male Holtzman rats received bilateral electrolytic lesions at the age of 26 days (Group 1), 59 days (Group 3), 75 days (Group 5) and 140 days (Group 7). Nonlesioned rats of the same age served as controls (Groups 2, 4, 6 and 8). The methods used were identical with those in the study on female rats. Table 1 shows that, while the body weight of 26-day-old rats was unaffected when compared with controls of the same age, the rats lesioned at older ages (Groups 3, 5 and 7) weighed significantly more than their controls after 6 weeks. In contrast, linear growth (body length, tail length) was reduced most in Group 1, less in Groups 3 and 5, and was unaffected in Group 7. It was slightly less (10 %) in males than in females (15%, Bernardis & Skelton, 1966). It is possible that the greater effect of ventromedial lesions in weanling rats is attributable to a greater vulnerability of the smaller brains in these animals. In terms of Lee's (1929) index, all rats were equally obese when compared with their respective controls, although only the rats of Groups 5 and 7 showed significant hyperphagia. The obesity in the weanling rats is in accord¬ ance with carcass fat determinations made by Han, Lin, Chu, Mu & Liu (1965). Since it is known that growth hormone (GH) has a lipolytic effect (Knobil & Hotchkiss, 1964) it is conceivable that a deficiency of this hormone at an early age results in a greater accumulation of adipose tissue than in non-deficient rats. The reduction in the number of the pituitary acidophils which are known to elaborate GH was signifi¬ cant and similar in Groups 1, 3 and 5 but insignificant in Group 7 when compared with their respective controls. This reduction was less in the weanling male (36 %) than in the weanling female (48 %) animals. The greatest reduction in organ weight occurred in the rats of Group 1. It is noteworthy that the heart (Beznak, 1960) and kidney (Astarabadi, 1963) are sensitive to GH and that the adrenals are thought to

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Growth and Obesity Following Ventromedial Hypothalamic Lesions Placed in Female Rats at Four Different Ages

Cited by 74 publications

References 9 publications

Origin of endocrine‐metabolic changes in the weanling rat ventromedial syndrome

Origin of endocrine‐metabolic changes in the weanling rat ventromedial syndrome

Effects of monosodium glutamate administration in the neonatal period on the diabetic syndrome in KK mice

Growth and Obesity in Male Rats After Placement of Ventromedial Hypothalamic Lesions at Four Different Ages

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