Development of hyperphagia in female rats with ventromedial hypothalamic lesions placed at four different ages

Bernardis, Lee L.; Bahorsky, Michael; Bohacek, Luise

doi:10.1007/bf01895273

Cited by 14 publications

(2 citation statements)

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“…However, the level of binding decreases slightly in cafeteria-fed rats between the fifteenth and thirtieth days of the experiment (50-65 d old) and it is during this time that cafeteria fed rats start to gain more weight than controls (Table 1). Other reports have noted that the body weights of cafeteria rats (Brooks et al 1981) and rats with lesions in the ventromedial hypothalamus (Bernardis, 1966) begin to diverge from controls at about 55-60 d of age and this has been ascribed to the fact that food intake is maximal in young stock-fed rats and thus hyperphagia and excess weight gain cannot occur. However, we have shown that this explanation is invalid since weanling cafeteria rats exhibit marked hyperphagia and the absence of obesity in these animals is due to a large, compensatory increase in energy expenditure (Brooks et al 1981).…”

Section: Discussionmentioning

confidence: 97%

Effects of Diet and Acute Noradrenaline Treatment on Brown Adipose Tissue Development and Mitochondrial Purine‐nucleotide Binding

1982

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Feeding rats a highly palatable 'cafeteria' diet resulted in a two-fold increase in interscapular brown adipose tissue (b.a.t.) mass after only 3 d on the diet. No significant difference in DNA content of b.a.t. was noted between control and cafeteria-fed rats at this time but DNA content was elevated 2-3-fold in the latter group by day 30, and incorporation rates of tritiated thymidine into DNA were elevated in these animals after 5, 15 and 30 d of cafeteria feeding. A doubling of specific GDP (per mg protein) to b.a.t. mitochondria was seen in cafeteria-fed rats on days 3, 15 and 30 and total GDP binding in the interscapular depot was increased by 3-4-fold. Injection of the animals with noradrenaline (25 micrograms/100 g body weight) 1 h before killing caused 180 and 430% increases in b.a.t. mitochondrial GDP binding in control and cafeteria-fed rats respectively. Linear Scatchard plots of binding data obtained from 15 d control and cafeteria groups indicated a single class of receptor, with the same affinity for GDP in all animals, but the maximum number of binding sites was markedly elevated in cafeteria rats and was increased further after treatment with noradrenaline 1 h prior to sacrifice. When cafeteria-fed rats were returned to stock diet alone the differences in b.a.t. mass and GDP binding diminished but after 10 d brown fat mass and noradrenaline-stimulated GDP binding were still significantly higher than control levels. These data provide further evidence for the involvement of b.a.t. and its mitochondrial proton conductance pathway in diet-induced changes in thermogenic capacity.

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Section: Discussionmentioning

confidence: 97%

Effects of Diet and Acute Noradrenaline Treatment on Brown Adipose Tissue Development and Mitochondrial Purine‐nucleotide Binding

1982

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“…Electrolytic, chemical, or genetic lesions of the ventromedial hypothalamic nucleus (VMH) result in obesity and hyperphagia, whereas lateral hypothalamic (LH) lesions result in weight loss and hypophagia (Owen et al, 1953;Marshall and Mayer, 1956;Bernardis et al, 1966;Majdic et al, 2002). These data formed the original basis for the dual-center hypothesis, which suggested that the LH functions as a feeding center, and the VMH functions as a satiety center.…”

Section: Introductionmentioning

confidence: 99%

Use of Laser-Capture Microdissection for the Identification of Marker Genes for the Ventromedial Hypothalamic Nucleus

Stallings²,

et al. 2005

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The ventromedial hypothalamic nucleus (VMH) plays an important role in the control of feeding and energy homeostasis. In contrast to other hypothalamic nuclei that are also known to regulate energy balance, there is a paucity of nucleus-specific marker genes for the VMH, limiting the application of molecular approaches for analyzing VMH information processing, function, and circuitry. Here, we report the use of laser-capture microdissection to isolate a set of cDNAs that are enriched in the VMH relative to two adjacent hypothalamic nuclei, the arcuate and dorsomedial hypothalamus. The relative expression levels of nine of the 12 most robustly expressed VMH-enriched genes were confirmed by real-time PCR analysis using separate RNAs from these three nuclei. Three of these VMH-enriched genes were further characterized by in situ hybridization histochemistry, including pituitary adenylate cyclase activating polypeptide, cerebellin 1, and an expressed sequence tag named LBH2. Finally, to test whether some of these genes were coordinately regulated, we monitored their expression in steroidogenic factor 1 (SF-1) knock-out mice. SF-1 is a transcription factor that controls the development of the VMH. The RNA levels for four of these genes were reduced in these knock-out animals, further suggesting that they are direct or indirect targets of this orphan nuclear receptor. The VMH-enriched genes identified here provide a basis for a functional analysis of VMH neuronal subpopulations via the use of bacterial artificial chromosome transgenics and related technologies. These results also demonstrate the utility of laser-capture microdissection coupled with microarray technology to identify nucleus-specific transcriptional networks.

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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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Development of hyperphagia in female rats with ventromedial hypothalamic lesions placed at four different ages

Cited by 14 publications

References 0 publications

Effects of Diet and Acute Noradrenaline Treatment on Brown Adipose Tissue Development and Mitochondrial Purine‐nucleotide Binding

Effects of Diet and Acute Noradrenaline Treatment on Brown Adipose Tissue Development and Mitochondrial Purine‐nucleotide Binding

Use of Laser-Capture Microdissection for the Identification of Marker Genes for the Ventromedial Hypothalamic Nucleus

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

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