Viewing the ventromedial hypothalamus from the adrenal gland

1984 ◽  
Vol 246 (1) ◽  
pp. R1-R12 ◽  
Author(s):  
M. F. Dallman
Keyword(s):  
Circadian Rhythm ◽  
Insulin Secretion ◽  
Food Intake ◽  
Adrenal Gland ◽  
Ventromedial Hypothalamus ◽  
Adrenocortical Function ◽  
Suprachiasmatic Nuclei ◽  
Inhibit Food Intake ◽  
Dose Dependent

The relationships among food intake, insulin secretion, and adrenocortical function are reviewed. It is hypothesized that a major role of structures in, or passing through, the ventromedial hypothalamus is to inhibit food intake, insulin secretion, and adrenocortical function during the day (in the nocturnally active rat) and that this activity is normally driven by elements within the suprachiasmatic nuclei. Lesions of the ventromedial hypothalamus of rats result in nonrhythmic food intake, hyperinsulinemia, nonrhythmic adrenocortical function, and obesity. Adrenalectomy prevents or reverses the effects of lesions of the ventromedial hypothalamus on food intake, insulin secretion, and obesity, and corticosteroid replacement restores them. Because the actions of corticosteroids are both time- and dose-dependent, it is proposed that the effects of the tonic levels of corticosteroids observed after lesions of the ventromedial hypothalamus are to augment the hyperphagia, hyperinsulinemia, and substrate flow into fat to a greater extent than would occur if there were a normal circadian rhythm in adrenocortical function.

The role of nitric oxide derived from l-arginine in the control of steroidogenesis, and perfusion medium flow rate in the isolated perfused rat adrenal gland

1993 ◽  
Vol 139 (3) ◽  
pp. 415-423 ◽  
Author(s):  
L. A. Cameron ◽  
J. P. Hinson
Keyword(s):  
Nitric Oxide ◽  
Adrenal Gland ◽  
Flow Rate ◽  
Adrenocortical Function ◽  
No Production ◽  
Percentage Increase ◽  
Perfusion Medium ◽  
Corticosterone Secretion ◽  
Dose Dependent

ABSTRACT The present studies were designed to investigate the role of nitric oxide (NO) in the regulation of adrenocortical function, using the intact rat adrenal gland in situ, perfused with medium (Hank's balanced salt solution) containing a range of concentrations of l-arginine, the substrate for NO production. In addition, the effects of NG-nitro-l-arginine methylester (l-NAME), an inhibitor of NO production, were investigated. Results showed that l-arginine caused a dose-dependent increase in the flow rate of the perfusion medium through the adrenal gland. This effect was specific, as neither d-arginine nor l-lysine had an effect. The presence of l-NAME (5 mmol/l) in perfusion medium containing l-arginine caused a decrease in flow rate to levels seen in the absence of l-arginine. In the presence of concentrations of l-arginine up to 500 μmol/l, corticosterone secretion rates were also stimulated in a dose-dependent manner. Further studies, investigating the effect of l-arginine on the response to ACTH(1–24) stimulation, found that the percentage increase in flow rate, aldosterone secretion and corticosterone secretion caused by ACTH were not significantly different using media containing 230 μmol l-arginine/l or in the absence of l-arginine. These results suggest a role for NO derived from l-arginine in the regulation of basal levels of adrenal vascular tone in the rat isolated adrenal gland preparation. They do not suggest an obligatory role for NO in either the vascular or steroidogenic response to ACTH stimulation. Journal of Endocrinology (1993) 139, 415–423

scholarly journals Role of Ventromedial Hypothalamus in Sucrose-Induced Obesity on Metabolic Parameters

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Metabolic Parameters ◽  
Male Rats ◽  
Significant Weight Gain ◽  
The Metabolic Syndrome

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.

Increased islet blood flow in obese rats: role of the autonomic nervous system

1992 ◽  
Vol 262 (5) ◽  
pp. E736-E740 ◽  
Author(s):  
N. Atef ◽  
A. Ktorza ◽  
L. Picon ◽  
L. Penicaud
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Ventromedial Hypothalamus ◽  
Zucker Rats ◽  
Islet Blood Flow ◽  
Obese Rats ◽  
Increased Sensitivity ◽  
Obese Zucker Rats

Hyperinsulinemia, a main feature of both human and animal obesity, has been demonstrated to be due to both an increased sensitivity to nutrient secretagogues and an impairment of the nervous regulation of insulin secretion. Recent studies have shown that pancreatic islet blood flow increases under conditions associated with an enhanced insulin secretion. The aim of this study was to determine whether or not changes in islet blood flow are present in hyperinsulinemic obese rats. Using the nonradioactive microsphere technique, we were able to show a significantly higher islet blood flow in obese rats either of the Zucker strain or Wistar rats after lesion of the ventromedial hypothalamus than in their respective lean controls. Subdiaphragmatic vagotomy had no significant effect on basal islet blood flow of lean rats, whereas it decreased significantly that of obese Zucker rats. Conversely, clonidine, an alpha 2-adrenergic agonist, induced a higher decrease of islet blood flow in obese than in lean Zucker rats. The injection of an intravenous bolus of glucose (375 mg/kg iv) increased significantly more islet blood flow in obese than in lean Zucker rats. It is concluded that obese rats present an increased pancreatic islet blood flow, which may result, at least in part, from exaggerated parasympathetic activity and lower than normal sympathetic activity. This could participate in the hyperinsulinemia observed in these rats.

scholarly journals The Antiobesity Effects of Centrally Administered Neuromedin U and Neuromedin S Are Mediated Predominantly by the Neuromedin U Receptor 2 (NMUR2)

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3101-3109 ◽  
Author(s):  
Andrea Peier ◽  
Jennifer Kosinski ◽  
Kimberly Cox-York ◽  
Ying Qian ◽  
Kunal Desai ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Central Administration ◽  
Diet Induced Obesity ◽  
Inhibit Food Intake ◽  
Selective Agonists ◽  
Treatment Of Obesity ◽  
The Brain ◽  
Deficient Mice

Neuromedin U (NMU) and neuromedin S (NMS) are structurally related neuropeptides that have been reported to modulate energy homeostasis. Pharmacological data have shown that NMU and NMS inhibit food intake when administered centrally and that NMU increases energy expenditure. Additionally, NMU-deficient mice develop obesity, whereas transgenic mice overexpressing NMU are lean and hypophagic. Two high-affinity NMU/NMS receptors, NMUR1 and NMUR2, have been identified. NMUR1 is predominantly expressed in the periphery, whereas NMUR2 is predominantly expressed in the brain, suggesting that the effects of centrally administered NMU and NMS are mediated by NMUR2. To evaluate the role of NMUR2 in the regulation of energy homeostasis, we characterized NMUR2-deficient (Nmur2−/−) mice. Nmur2−/− mice exhibited a modest resistance to diet-induced obesity that was at least in part due to reduced food intake. Acute central administration of NMU and NMS reduced food intake in wild-type but not in Nmur2−/− mice. The effects on activity and core temperature induced by centrally administered NMU were also absent in Nmur2−/− mice. Moreover, chronic central administration of NMU and NMS evoked significant reductions in body weight and sustained reductions in food intake in mice. In contrast, Nmur2−/− mice were largely resistant to these effects. Collectively, these data demonstrate that the anorectic and weight-reducing actions of centrally administered NMU and NMS are mediated predominantly by NMUR2, suggesting that NMUR2-selective agonists may be useful for the treatment of obesity.

scholarly journals Modulation of crayfish retinal function by red pigment concentrating hormone

1995 ◽  
Vol 198 (7) ◽  
pp. 1447-1454 ◽  
Author(s):  
A Garfias ◽  
L Rodríguez-Sosa ◽  
H Aréchiga
Keyword(s):  
Circadian Rhythm ◽  
Light Adaptation ◽  
Retinal Pigment ◽  
Physiological Role ◽  
Pigment Cells ◽  
Red Pigment ◽  
Retinal Activity ◽  
Retinal Photoreceptors ◽  
Dose Dependent

The role of the crustacean octapeptide red pigment concentrating hormone (RPCH) in the control of crayfish retinal activity was explored. RPCH injection into intact animals resulted, after a latency of 10­30 min, in a dose-dependent enhancement of electroretinogram (ERG) amplitude lasting 60­120 min. RPCH was able to potentiate ERG amplitude in both light-adapted and dark-adapted animals. Following light-adaptation, responsiveness to RPCH was five times higher than following dark-adaptation. In conjunction with ERG enhancement, in light-adapted animals, RPCH injection elicited a dose-dependent retraction of distal retinal pigment, but did not affect proximal retinal pigment position. The effects of RPCH were blocked by a polyclonal antibody raised against a tyrosinated form of RPCH (A-tyr-RPCH). The antibody was also capable of partially blocking the nocturnal phase of the circadian rhythm of ERG amplitude and the darkness-induced retraction of distal retinal pigment. These results suggest that RPCH acts both on the retinal photoreceptors and on the distal pigment cells, playing a physiological role as a mediator of the effects induced by darkness and by the nocturnal phase of the circadian rhythm.

Rapid synthesis and secretion of intestinal apolipoprotein A-IV after gastric fat loading in rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1170-R1177 ◽  
Author(s):  
M. D. Rodriguez ◽  
T. J. Kalogeris ◽  
X. L. Wang ◽  
R. Wolf ◽  
P. Tso
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Intragastric Administration ◽  
Short Term ◽  
Apolipoprotein A ◽  
Inhibit Food Intake ◽  
Rapid Stimulation ◽  
Kinetics Of ◽  
Distal Jejunum

To further investigate the possible role of apolipoprotein A-IV (apo A-IV) in the short-term control of food intake, we examined the kinetics of intestinal apo A-IV synthesis and release into lymph and plasma after intragastric delivery of physiological amounts of lipid. Within 30 min of intragastric administration of 0.1 g of triglyceride, plasma and lymph levels of apo A-IV were similar to those produced by exogenous apo A-IV that inhibit food intake. Within 15 min, 5% of gastrically delivered radioactive lipid reached the distal small bowel and cecum; by 30 min radioactivity was evenly distributed throughout the small intestine, with 10-15% of the load in the distal gut. By 30 min, synthesis of apo A-IV was significantly stimulated in proximal and distal jejunum and distal ileum and remained elevated up to 4 h after the delivery of lipid. Our results indicate that the delivery of physiological amounts of lipid into the stomach produces a significant and rapid stimulation of apo A-IV secretion into lymph and plasma, together with a rapid delivery of lipid and increases in mucosal synthesis of apo A-IV along the entire length of the small intestine. The results support a possible role for apo A-IV in the short-term control of food intake and suggest a role for the entire gut in the integrative response of apo A-IV to a fat meal.

Fourth ventricle bombesin injection suppresses ingestive behaviors in rats

1989 ◽  
Vol 256 (3) ◽  
pp. R590-R596 ◽  
Author(s):  
F. W. Flynn
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Fourth Ventricle ◽  
Home Cage ◽  
Saline Injection ◽  
Bottle Test ◽  
Inhibit Food Intake ◽  
Ingestive Behaviors ◽  
Intact Rats

Food intake after fourth intracerebroventricular (icv) injections of bombesin (BBS) was measured in intact rats. BBS injections (greater than or equal to 10 ng) reliably suppressed chow intake in 17-h food-deprived rats. Systemic injections of BBS (50 ng) had no effect on food intake. These data indicate that BBS can act directly on caudal brain stem site(s) to inhibit food intake. The behavioral specificity of fourth icv BBS was evaluated by measuring the effects of fourth icv BBS injection on water intake by 17-h water-deprived rats in the presence and absence of food. Fourth icv injections of BBS in doses greater than 10 ng suppressed 30-min and 2-h water intake relative to saline injection when food was available in the home cage. In contrast, when food was not present during the 2-h intake test, fourth icv injections of BBS had no effect on water intake. This suggests that the inhibition of water intake was secondary to the effects of BBS on food intake. Lastly, sucrose (0.1 M) was paired with fourth icv BBS (50 ng), fourth icv saline, and intraperitoneal LiCl (1.5 meq/kg) in three groups of naive rats, and sucrose preference was subsequently measured. Rats that received injections of either saline or BBS preferred sucrose during the 24-h two-bottle test, and their preference ratios were significantly greater than those of the LiCl-injected rats. The role of afferent signals elicited by fourth ventricle BBS administration in the control of food intake is discussed.

scholarly journals Cholecystokinin and D-fenfluramine inhibit food intake in oxytocin-deficient mice

2003 ◽  
Vol 285 (5) ◽  
pp. R1037-R1045 ◽  
Author(s):  
Rose C. Mantella ◽  
Linda Rinaman ◽  
Regis R. Vollmer ◽  
Janet A. Amico
Keyword(s):  
Food Intake ◽  
Neural Pathways ◽  
Dependent Manner ◽  
Similar Extent ◽  
Laboratory Rats ◽  
Inhibit Food Intake ◽  
Fos Expression ◽  
The Relationship ◽  
Dose Dependent ◽  
Deficient Mice

Results from previous studies indicate that oxytocin (OT)-containing neural pathways are activated in laboratory rats after systemic administration of CCK or d-fenfluramine and that centrally released OT may participate in the anorexigenic effects of these treatments. To explore the relationship between feeding behavior and OT function, the effects of CCK and d-fenfluramine on feeding and central c-Fos expression were compared in wild-type (OT+/+) and OT-deficient mice (OT-/-) of C57BL/6 background. Male OT+/+ and OT-/- mice were administered saline or CCK (1, 3, or 10 μg/kg ip) after overnight food deprivation. Saline-treated OT+/+ and OT-/- mice consumed equivalent amounts of food after an overnight fast. CCK inhibited deprivation-induced food intake in a dose-dependent manner to a similar extent in both genotypes. CCK treatment also induced similar hindbrain and forebrain patterns of increased c-Fos expression in mice of both genotypes. After treatment with d-fenfluramine (10 mg/kg ip), both OT+/+ and OT-/- mice consumed significantly less food than untreated controls, with no difference between genotypes. We conclude that OT signaling pathways are unnecessary for the anorexigenic effects of systemically administered CCK and d-fenfluramine in C57BL/6 mice.

Hypothalamic hyperinsulinemia and obesity: role of adrenal glucocorticoids

1983 ◽  
Vol 245 (2) ◽  
pp. E194-E199
Author(s):  
B. M. King ◽  
A. R. Banta ◽  
G. N. Tharel ◽  
B. K. Bruce ◽  
L. A. Frohman
Keyword(s):  
Insulin Secretion ◽  
Food Intake ◽  
Plasma Insulin ◽  
Female Rats ◽  
Hypothalamic Obesity ◽  
Previous Conclusion ◽  
Glucose Levels ◽  
Corticosterone Treatment ◽  
Adrenalectomized Rats

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.

scholarly journals Activation of the NPY Y5 receptor regulates both feeding and energy expenditure

1999 ◽  
Vol 277 (5) ◽  
pp. R1428-R1434 ◽  
Author(s):  
Joyce J. Hwa ◽  
Melanie B. Witten ◽  
Patricia Williams ◽  
Lorraine Ghibaudi ◽  
Jun Gao ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Interscapular Brown Adipose Tissue ◽  
Peptide Analogs ◽  
Brown Adipose ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Intracerebroventricular (ICV) administration of neuropeptide Y (NPY) has been shown to decrease energy expenditure, induce hypothermia, and stimulate food intake. Recent evidence has suggested that the Y5 receptor may be a significant mediator of NPY-stimulated feeding. The present study attempts to further characterize the role of NPY Y5-receptor subtypes in feeding and energy expenditure regulation. Satiated Long-Evans rats with temperature transponders implanted in the interscapular brown adipose tissue (BAT) displayed a dose-dependent decrease in BAT temperature and an increase in food intake after ICV infusion of NPY. Similar effects were induced by ICV administration of peptide analogs of NPY that activate the Y5 receptor, but not by analogs that activate Y1, Y2, or Y4 receptors. Furthermore, ICV infusion of the Y5 selective agonistd-[Trp32]-NPY significantly reduced oxygen consumption and energy expenditure of rats as measured by indirect calorimetry. These data suggest that the NPY Y5-receptor subtype not only mediates the feeding response of NPY but also contributes to brown fat temperature and energy expenditure regulation.

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