Medial hypothalamic serotonin in the control of eating behavior.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
G Shor-Posner
Publications and source records attributed to G Shor-Posner.
Destruction of noradrenergic innervation to the paraventricular nucleus: deficits in food intake, macronutrient selection, and compensatory eating after food deprivation.
Norepinephrine (NE) injected into the paraventricular nucleus (PVN) has a stimulatory effect on feeding behavior and is found to selectively enhance preference for carbohydrate in the rat. The present experiments were conducted to assess the impact of chronic depletion of NE within the PVN on food intake and appetite regulation. The catecholamine (CA) neurotoxin, 6-hydroxydopamine (6-OHDA), when administered into the PVN, produced a significant depletion of PVN NE in association with a variety of behavioral changes. The immediate consequence of the neurotoxin lesion was a dramatic increase in 24-hr food intake, attributed predominantly to a preferential increase in carbohydrate and fat consumption. The long-term effects related to CA depletion were a deficit in daily food consumption, particularly of carbohydrate (-42%). Although animals with diminished PVN NE maintained a normal diurnal feeding pattern, they failed to exhibit the increased ingestion of an energy-rich carbohydrate diet which rats normally show during the dark period of the diurnal cycle. Rats injected with 6-OHDA directly into the PVN exhibited a normal response to glucoprivic challenge, but demonstrated a deficit in their ability to produce compensatory feeding, particularly of carbohydrate and fat, in response to food deprivation. These findings suggest a specific function for PVN noradrenergic mechanisms in normal energy repletion when body energy stores are reduced.
Adaptation, Physiological↗
Morphine-stimulated feeding: analysis of macronutrient selection and paraventricular nucleus lesions.
The hypothalamic paraventricular nucleus (PVN) has been found to be sensitive to the feeding stimulatory effects of opiates. The present experiments investigated the effect of systemic morphine (2 mg/kg) on macronutrient selection in freely-feeding and food-restricted rats and assessed the impact of PVN electrolytic and 6-hydroxydopamine lesions on the rats' ability to respond to peripheral morphine injection. In satiated rats, maintained ad lib on pure macronutrient diets, morphine increased food intake. This effect was associated with a preferential increase in protein ingestion; carbohydrate consumption, compared with fat and protein intake, was least affected. In food-restricted rats, permitted to eat for 6 hr, morphine instead produced a particular preference for fat, with no significant enhancement of total calorie intake. While PVN 6-hydroxydopamine lesions, which depleted PVN catecholamine levels by 70%, failed to alter morphine-stimulated feeding, electrolytic lesions of the PVN significantly attenuated this response, particularly protein and fat ingestion. This suggests that opiate-induced feeding may, in part, be mediated through the PVN, which is known to have an important function in the control of food ingestion.
Animals↗
Hypothalamic serotonin in the control of meal patterns and macronutrient selection.
Serotonin (5-HT) is believed to have an inhibitory influence over feeding behavior. The present experiments were designed to investigate the effects of hypothalamic 5-HT on spontaneously motivated feeding and appetite regulation. Freely-feeding rats were injected with 5-HT or norfenfluramine (NORFENF) directly into the paraventricular hypothalamus (PVN), and precise changes in feeding behavior were monitored by a computer. Following PVN 5-HT or NORFENF injection, animals exhibited a marked suppression in food intake, associated with a decrease in meal size, duration and eating rate, and no change in the frequency of meals consumed. This suggests that brain 5-HT may influence primarily the induction of satiety rather than the suppression of hunger. The effect of drugs presumed to affect brain 5-HT transmission on diet selection was also investigated in groups of rats injected centrally with 5-HT or NORFENF or peripherally with either fenfluramine, quipazine or cyproheptadine. In a series of 2-diet tests, rats centrally injected with 5-HT or NORFENF exhibited a selective suppression of the carbohydrate-rich diets. In animals provided with three pure macronutrient diets, protein, carbohydrate, and fat, systemic administration of serotonergic agents had its greatest impact on fat and carbohydrate ingestion, as compared to protein consumption. These findings support a role for hypothalamic 5-HT in modulating meal patterns and appetite for particular macronutrients.
Animals↗
Amphetamine: effects on meal patterns and macronutrient selection.
Catecholaminergic systems, specifically in the region of the lateral perifornical hypothalamus (PFH), have been linked to the inhibition of feeding behavior. The present studies examined the effects of d-amphetamine (AMPH), which is believed to act through the release of endogenous catecholamines (CAs), on spontaneous feeding and appetite regulation in rats. Injection of AMPH directly into the PFH caused a marked suppression of food intake; changes in computer-monitored meal patterns were characterized by an increase in the latency to meal onset and a consequent reduction in meal size and duration. This suggests that hypothalamic AMPH administration may influence primarily the initiation, rather than the termination, of feeding. In other experiments, chronic infusion of AMPH directly into the PFH was shown to suppress 24 hr food intake and body weight gain, indicating the effectiveness of lateral hypothalamic CA stimulation in overriding normal long-term patterns of feeding. The effect of hypothalamic CA stimulation on macronutrient selection was also investigated in groups of rats injected either centrally or peripherally with AMPH, or centrally with the CA agonists, dopamine and epinephrine. Each of these manipulations caused a strong inhibition of protein intake with no effect on carbohydrate, and only a mild suppression of fat ingestion after peripheral AMPH. These selective effects of AMPH on feeding patterns and diet choice, provide support for a role of CA innervation to the lateral hypothalamus in the modulation of natural feeding behavior and macronutrient selection.
Animals↗
Brain serotonin and eating behavior.
Studies indicate that hypothalamic monoamine systems involved in the control of food intake have specific effects on temporal feeding patterns and on appetite for specific macronutrients. Based on the evidence obtained in rats, it is proposed that serotonin acts, in part, through a satiety mechanism of the medial hypothalamus, to reduce ingestion of carbohydrate while sparing protein intake. In controlling the ratio of carbohydrate to protein intake, this serotonergic system, which is responsive to the anorectic agent fenfluramine, is believed to function in direct opposition to the alpha 2-noradrenergic system of the paraventricular nucleus, which inhibits satiety for carbohydrate and thereby potentiates the size of carbohydrate meals. This serotonergic system may also indirectly oppose the catecholaminergic systems of the lateral hypothalamus, which mediate amphetamine anorexia and which inhibit a hunger-stimulating system for protein intake, thereby delaying the initiation of protein meals. Examination of the rats' normal eating patterns, in conjunction with particular biochemical analyses, has indicated specific points in the circadian eating cycle where these hypothalamic monoamine systems, in association with changes in circulating hormones and nutrients, may be physiologically activated.
Amphetamine↗
Deficits in the control of food intake after hypothalamic paraventricular nucleus lesions.
Noradrenergic mechanisms of the hypothalamic paraventricular nucleus (PVN) have been shown to play an important role in the stimulation of feeding To determine the influence of this nucleus in monitoring and controlling responses to physiological and pharmacological challenges, PVN electrolytic lesion rats were tested for their behavioral responsiveness to agents known to affect the alpha-2 noradrenergic system as well as release of corticosterone, and to short- and long-term periods of food deprivation. Discrete lesions of the PVN produced enhanced feeding, particularly of carbohydrate, in freely-feeding rats maintained on a macronutrient self-selection paradigm. Lesion rats demonstrated a behavioral deficit in food intake regulation (a decrease in carbohydrate ingestion) in response to 5-hr and 24-hr fasts, showed a disturbance in circadian feeding, and exhibited a dramatic decrease in circulating corticosterone. However, feeding in response to 2-deoxy-D-glucose and insulin remained intact, suggesting that noradrenergic receptors within the PVN are not involved in the mediation of glucoprivic-induced feeding.
Animals↗
Role of hypothalamic norepinephrine in control of meal patterns.
Feeding behavior has been shown to be strongly affected by central administration of catecholamines. In this study, we examined in freely-feeding rats the effect of hypothalamic norepinephrine (NE) injections on the basic parameters of spontaneous ingestion. Precise changes in feeding behavior in rats maintained on ad lib food and water intake were monitored by a PDP 8 computer connected to an apparatus capable of measuring licks and bites of food. Injections of NE were administered into the hypothalamic paraventricular nucleus, the most sensitive brain area for the elicitation of feeding through direct alpha-noradrenergic stimulation. In tests conducted under both light and dark conditions, NE facilitated food intake, primarily by an increase in meal size rather than meal frequency. The first meal after injection was increased in size and duration; the rate of eating was also enhanced. Whereas the following intermeal interval was significantly larger, subsequent meals and intermeal intervals appeared generally unaffected. This evidence is consistent with the proposal of a role for hypothalamic NE in the maintenance, rather than initiation, of feeding behavior in freely-feeding rats.
Animals↗
Nutritional alterations in HIV-1 seropositive and seronegative drug users.
Explore the source record for details and available documents.
HIV Seronegativity↗
Plasma pyridoxine deficiency is related to increased psychological distress in recently bereaved homosexual men.
OBJECTIVE: Previous research has demonstrated that a theoretical model including measures of life stressors, social support, and coping style significantly predicts psychological distress. This study tested plasma pyridoxine (vitamin B6) deficiency status as a predictor of overall psychological distress and specific mood states in this model, controlling for HIV-1 serostatus. METHOD: Subjects included HIV-1+ (N = 76) and HIV-1- (N = 58) recently bereaved homosexual men. At baseline, subjects completed a battery of psychosocial questionnaires, together with a physical examination and venipuncture. The Profile of Mood States (POMS) provided measures of overall psychological distress as well as specific mood states. Pyridoxine deficiency status (a categorical measure of deficient vs. adequate status) was determined with a bioassay of erythrocyte aspartate aminotransferase activity. RESULTS: Pyridoxine deficiency was a significant predictor of increased overall psychological distress in this model, controlling for life stressors, social support, coping style, and HIV-1 serostatus. In post hoc analyses of specific mood state effects, pyridoxine deficiency status was significantly associated with increases in depressed, fatigued, and confused mood levels, but not with those of anxiety, anger, or vigor. DISCUSSION: These findings suggest that adequate pyridoxine status may be necessary to avert psychological distress in the setting of bereavement. Inasmuch as pyridoxine is a cofactor for 5-hydroxytryptophan decarboxylase--an enzyme in the biosynthesis pathway of serotonin--serotonin level in the brain is implicated as the mediating factor.
Adaptation, Psychological↗
Selenium status of HIV-1 infected individuals.
Explore the source record for details and available documents.
Acquired Immunodeficiency Syndrome↗
Inadequate dietary intake and altered nutrition status in early HIV-1 infection.
Recent studies indicate that multiple nutritional abnormalities occur relatively early in the course of human immunodeficiency virus (HIV-1) infection. Decreased plasma levels of vitamins B6, B12, A, and E and zinc have been correlated with dietary intake and associated with significant alterations in immune response and cognitive function. To determine the level of intake consistent with normal plasma nutrient levels, we examined nutrition status in relation to food consumption and nutrient supplementation in HIV-1-seropositive (HIV+) and -seronegative (HIV-) homosexual men. The mean level of total intake (diet plus supplements) for all nutrients was significantly higher in HIV+ men. To achieve normal plasma nutrient values, the HIV+ men appeared to require intake in multiples of the recommended dietary allowance (RDA) for vitamins A, E, B6, and B12 and zinc. For the HIV+ men, a relatively high proportion of biochemical deficiency was associated with consumption of vitamin B6 and zinc at the RDA level. Because little evidence of deficiency was observed with elevated intake in both groups, an effective program of nutritional supplementation may be beneficial in maintaining adequate plasma nutrient levels.
Adult↗