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Biomedical subjects

B M King

Publications and source records attributed to B M King.

At least 55 records · Page 3Linked to original sources
PubMed1985

Hypothalamic obesity after hypophysectomy or adrenalectomy: dependence on corticosterone.

Recent studies have found that the hyperphagia and obesity resulting from lesions of the ventromedial hypothalamus (VMH) are both reversed and prevented by complete adrenalectomy. Several previous experiments, however, reported little or no suppression of VMH weight gain in hypophysectomized (HYPOX) rats. This study directly compared the effects of hypophysectomy and adrenalectomy on hypothalamic obesity in adult female rats. Complete adrenalectomy (i.e, stress-induced plasma corticosterone less than 1.0 micrograms/dl) totally suppressed abnormal weight gain in the first 20 days after VMH lesions but did not affect intracranial self-stimulation. Hypophysectomy also resulted in suppression of weight gain, but the HYPOX-VMH rats nevertheless gained significantly more weight than HYPOX rats with sham lesions. However, the HYPOX-VMH animals had very low levels of plasma corticosterone and adrenocorticotropin (ACTH) (from residual pituitary tissue or of diencephalic origin), and incompletely adrenalectomized rats with similar low levels of plasma corticosterone gained an equal amount of weight after VMH lesions. It was concluded that adrenal glucocorticoid hormones play a largely permissive role in the VMH syndrome, with only very small levels required for the manifestation of obesity.

Adrenalectomy↗
PubMed1985

Morphology of bluetongue virus-infected Aedes albopictus (C6/36) cell culture.

Morphological changes observed in bluetongue virus (BTV)-infected Aedes albopictus (C6/36) suspension cell culture at 28 C were compared to those observed in mammalian stationary cell culture at 37 C. The presence of cytoplasmic macrotubules, viroplasms and progeny virions was confirmed and appears to be the same as seen in mammalian cell culture. In addition progeny virions were observed budding from cell membranes where they appeared to acquire a lipoprotein envelope. Intranuclear macrotubules that are the same diameter as the cytoplasmic macrotubules were also seen. C6/36 cell culture is a model for gaining insight into BTV-replication in the insect host.

Aedes↗
PubMed1984

Relationship between plasma corticosterone and insulin levels in rats with ventromedial hypothalamic lesions.

The effects of ventromedial hypothalamic (VMH) lesions on plasma corticosterone, insulin, and glucose levels were studied in food-restricted and ad lib fed female rats. VMH lesions resulted in significant elevations of corticosterone and insulin levels compared to control values during the first 25 days after surgery. However, unlike insulin values which were generally greater in VMH rats fed ad lib than in food-restricted animals, plasma corticosterone levels were unaffected by level of food intake. Corticosterone and insulin levels were unrelated preoperatively and in sham-operated animals, but were positively correlated (r = .82) by Day 25 in ad lib fed VMH rats. It is concluded that the elevation in plasma glucocorticoids observed in VMH rats is a primary effect of the lesion that is independent of food intake or initial weight gain.

Animals↗
PubMed1984

Hyperinsulinemia in rats with ventromedial hypothalamic lesions: role of hyperphagia.

The relation of hyperinsulinemia to hyperphagia was examined in rats with lesions of the ventromedial hypothalamus (VMH). Plasma insulin and glucose levels were assayed after a 4-hr fast and 17 min after the initiation of a meal (6 ml of sweetened milk in 7 min) in animals with sham lesions, VMH animals maintained at preoperative body weight by food restriction, and VMH animals fed ad lib. Both VMH groups displayed basal and postabsorptive hyperinsulinemia, compared with the sham-operated control group, but insulin levels were greatest under the ad lib feeding condition. It is suggested that VMH hyperinsulinemia is due both to a primary effect of the lesion and to hyperphagia and that marked obesity can result in the absence of basal hyperinsulinemia as a result of hyperphagia with consequent postabsorptive hyperinsulinemia.

Animals↗
PubMed1983

Hypothalamic hyperinsulinemia and obesity: role of adrenal glucocorticoids.

The effects of adrenalectomy on the obesity and hyperinsulinemia induced by ventromedial hypothalamic (VMH) lesions were studied in female rats. Plasma insulin and glucose levels were assayed after a 4-h fast and 17 min after the initiation of a meal (6 ml sweetened milk in 7 min). The development of hypothalamic obesity was prevented by prior adrenalectomy and restored by administration of corticosterone. Adrenalectomy abolished both the basal and postabsorptive hyperinsulinemia observed in sham-adrenalectomized rats with VMH lesions. Corticosterone treatment of adrenalectomized animals enhanced both basal and postabsorptive insulin levels, but adrenalectomized rats with VMH lesions were hyperinsulinemic compared with animals with sham lesions only under the postabsorptive condition. Postabsorptive glucose levels were unaffected by either the lesion or adrenal ablation. The results support our previous conclusion that postabsorptive hyperinsulinemia is of greater importance than is basal hyperinsulinemia in the pathogenesis of hypothalamic obesity. Although the results are consistent with a stimulatory role of corticosterone on food intake mediating the postabsorptive hyperinsulinemia, a primary effect on CNS loci involved with the regulation of insulin secretion is also possible.

Adrenalectomy↗
PubMed1982

Naloxone decreases consumption of liquid and solid sucrose in vagotomized rats.

Intraperitoneal injections of the opiate antagonist naloxone decreased food intake in both vagotomized and sham-vagotomized rats. Consumption of liquid and solid sucrose, which were used in order to equate baseline intake, was equally suppressed in both groups under food-deprivation and appetitively-motivated conditions at all doses of naloxone (1, 2, 4, and 8 mg/kg). It is concluded that, in contrast to previous findings, the vagus nerve does not mediate the suppressive effects of naloxone on feeding behavior.

Animals↗
PubMed1982

The role of vagally-medicated hyperinsulinemia in hypothalamic obesity.

Evidence that the obesity syndrome which follows ventromedial hypothalamic (VMH) lesions is at least partially the result of a primary metabolic dysfunction is reviewed, as are proposals that the altered metabolism is due to enhanced vagally-mediated insulin release. This hypothesis was based largely on experiments demonstrating the complete reversal of hypothalamic obesity by subdiaphragmatic vagotomy, but subsequent studies have revealed that hypothalamic obesity is not always prevented by prior vagal transections. Interpretation of these discrepant results has been made difficult because of the frequent use of gastric secretion, behavioral, or other indirect tests for completeness of vagotomy. A review of more recent studies which have employed either direct assessment of vagotomy effects on insulin levels, pharmacological blockade of vagal efferent activity, or selective vagotomies indicates that vagally-mediated hyperinsulinemia can account for no more than 40% of the weight gain observed in animals with VMH lesions fed ad libitum, and may not be involved in the obesity that results from some parasagittal VMH knife cuts. It is concluded that vagally-mediated hyperinsulinemia does make a substantial, although not exclusive, contribution to the increased carcass lipid content observed in VMH animals that are food-restricted or pair-fed with control animals.

Animals↗
PubMed1982

Adrenocortical response to hypertonic saline in rats with lateral hypothalamic lesions.

Plasma corticosterone levels were used to assess the response to stress induced by intraperitoneal injections of hypertonic saline in rats with lateral hypothalamic (LH) or sham lesions. Rats with LH lesions displayed a corticosterone response equal to that of normal animals under basal conditions, after control injections of isotonic saline, and 20 min after injection of hypertonic saline (1.5 M, 1.0 ml/100 g of body weight). The corticosterone response of animals with LH lesions, however, was significantly less than that of normal animals 90 min after injection of hypertonic saline when no water was available. With access to water, normal animals displayed substantial drinking (14.5 ml/90 min), which resulted in a reduction in plasma corticosterone concentrations to a level observed after a control injection of isotonic saline, but the little water ingested by animals with LH lesions (2.5 ml) had no effect on the pituitary-adrenal system. It is concluded that the failure of animals with LH lesions to drink following a hydrational challenge is not the result of an exaggerated response to stress.

Adrenal Cortex↗
PubMed1982

Effects of adrenalectomy and corticosterone administration on hypothalamic obesity in rats.

The present experiment was designed to assess the role of adrenal hormones in hypothalamic hyperphagia and obesity. Ventromedial hypothalamic (VMH) or sham lesions were produced either 15 days before or after adrenalectomy (ADX) or sham adrenalectomy in rats in a completely counterbalanced design (experiment 1). Body weight and food intake were recorded for 30 days after the second surgery. Adrenalectomy in obese VMH animals eliminated all excess weight gain and decreased food intake to below the level of all control groups. VMH lesions in ADX animals did not produce the characteristic weight gain associated with ventromedial hypothalamic damage, and this group was not significantly different from animals with sham lesions in body weight or food intake. In experiment 2, the administration of corticosterone resulted in a marked increase in the rate of weight gain in ADX-VMH animals, and the withdrawal of the hormones was followed by weight loss. It is concluded that adrenal glucocorticoid hormones are necessary for the development and maintenance of VMH hyperphagia and obesity.

Adrenal Glands↗
PubMed1980

A re-examination of the ventromedial hypothalamic paradox.

Early studies of hypothalamic function found that damage to the ventromedial hypothalamus (VMH) resulted in marked overeating but inferior performance in food-motivated tasks, leading several investigators to conclude that hyperphagic VMH animals were actually less hungry than normal animals. However, numerous studies have since demonstrated that under certain conditions VMH-damaged animals will work as hard or harder for food, and consume as much or more of an unpalatable diet, than normal animals. A review of these experiments suggests that most of the deficits in food-motivated behavior are the result of two dysfunctions, one obesity induced, and the other a direct result of the lesion that can be greatly alleviated by preoperative adaptation. Explanations of the VMH paradox are also examined, and it is concluded that most are too narrow in scope, generally ignoring the fact that obesity and preoperative adaptation have similar effects on thirst- and some avoidance-motivated behaviors. It is proposed that the impaired performance of VMH-lesioned animals in food-reinforced tasks is largely the result of obesity- and lesion-induced dysfunctions that are not specific to either hunger- or thirst-motivated behaviors.

Animals↗
PubMed1980

MIF-I suppresses deprivation-induced fluid consumption in rats.

Rats were injected IP with a 0.1 mg/kg dose of MIF-I, naloxone, dynorphin, [D-Phe4]-Met-enkephalin, [D-Ala2, F5Phe4]-Met-enkephalin-NH2, or the diluent vehicle, placed in their home cages for ten minutes, and then given ad lib access to either 20% sucrose, 10% sucrose, water, 0.01% quinine, or 0.02% quinine in a repeated measures design with solutions counter-balanced over five days. Fluid consumption was measured very hour for 4 hours. A mixed analysis of variance yielded significant results for all main effects and the peptides by fluid and hours by fluid interactions. For the 4-hr test period, naloxone and [D-Phe4]-Met-enkephalin produced reliable increased in consumption while MIF-I produced a reliable decrease. Differences were obtained only with sucrose solutions, and the results clearly suggest that peptides modulate fluid consumption at positive levels of incentive motivation. To reconcile the findings of increased consumption after naloxone with the many studies suggesting a decrease in such paradigms, 0.1, 1.0, and 10.0 mg/kg of naloxone and MIF-I were administered as before but to independent groups of rats and intake was measured every 30 min. These results replicate and extend the above findings by showing that during the first 30-min period, both naloxone and MIF-I suppressed intake in a dose-dependent fashion, with MIF-I being more effective at each dose. The 0.1 mg/kg naloxone group, however, increased consumption over time and achieved a total consumption greater than control animals but comparable to that observed in the first study. It appears that at very low doses naloxone increases consumption over time, but at more commonly tested higher doses it has a suppressant effect. The results support the concept that in many situations MIF-I can produce the same effects as naloxone.

Animals↗
PubMed1980

Hypothalamic obesity in female rats in absence of vagally mediated hyperinsulinemia.

In order to assess the role of vagally mediated hyperinsulinemia in hypothalamic obesity, plasma insulin and glucose levels were assayed in vagotomized and sham-vagotomized female rats after a 6-h fast and after a measured glucose meal both before and 10-14 days after ventromedial hypothalamic (VMH) lesions. Both groups displayed similar gains in body weight in the first 10 days after VMH lesions, but only the sham-vagotomized VMH-lesioned animals displayed elevated fasting insulin levels. Fasting glucose levels did not differ either before or after the lesion. The insulin response to oral glucose was increased in VMH rats, both in vagotomized and sham-vagotomized animals, and it is concluded that the hyperresponsiveness to oral glucose is independent of vagal mediation. Vagotomy markedly exaggerated the glucose and insulin response to oral glucose loading in both intact rats and rats with VMH lesions, probably as a result of more rapid absorption of glucose from the intestine. It is concluded that the fasting hyperinsulinemia that is characteristic of VMH animals is under vagal control and that its elimination does not prevent the development of obesity.

Animals↗
PubMed1979

Naloxone-induced suppression of food intake in normal and hypothalamic obese rats.

Intraperitoneal injections of naloxone hydrochloride (1, 2, 4, and 8 mg/kg) suppressed food intake in both normal and hypothalamic obese rats maintained on a 4-hr per day feeding schedule. The decrease in feeding was more pronounced in the animals with ventromedial hypothalamic lesions. Appetitively motivated feeding, i.e., the consumption of sweetened milk under nondeprived conditions, was also suppressed by naloxone, but there was no reliable difference between groups. It is concluded that opiate receptors located in the ventromedial hypothalamus are not essential for the effects of opiate agonists and antagonists on feeding behavior.

Animals↗