Failure to demonstrate disruption of ultradian growth hormone rhythm and insulin secretion by dorsomedial hypothalamic nucleus lesions that cause reduced body weight, linear growth and food intake

1987 ◽  
Vol 66 (3) ◽  
pp. 572-576 ◽  
Author(s):  
L. L. Bernardis ◽  
G. S. Tannenbaum
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Insulin Secretion ◽  
Food Intake ◽  
Linear Growth ◽  
Hypothalamic Nucleus ◽  
Reduced Body ◽  
Dorsomedial Hypothalamic Nucleus

Effect of dorsomedial hypothalamic nuclei knife cuts on ingestive behavior

1999 ◽  
Vol 276 (6) ◽  
pp. R1772-R1779 ◽  
Author(s):  
Larry L. Bellinger ◽  
Lee L. Bernardis
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Water Deprivation ◽  
Linear Growth ◽  
Ingestive Behavior ◽  
Hypothalamic Nucleus ◽  
Feeding System ◽  
Reduced Body ◽  
Hypothalamic Nuclei ◽  
Dorsomedial Hypothalamic Nucleus

Previous findings show that rats with electrolytic or excitotoxic lesions in the dorsomedial hypothalamic nucleus (DMN) are hypophagic and hypodipsic and have reduced ponderal and linear growth but normal body composition. DMN-lesioned (DMNL) rats also show altered ingestive responses to naloxone. The present study investigated the intrahypothalamic nerve pathways involved in these DMNL effects and the response of the pathways to deprivation challenges by placing knife cuts posterior (Post), lateral (Lat), ventral (Vent), dorsal, or anterior to the DMN or by administering sham operations. One major finding was that rats with Post or Vent were hypophagic ( P < 0.05) and had reduced body weight but responded normally to deprivation challenges. Post and Lat groups were hypodipsic ( P < 0.05), but plasma Na+, K+, and osmolality and 24-h post-water-deprivation drinking responses were similar in all groups. Naloxone did not suppress the intake of Post rats. It appears that the hypophagia and the reduced body weight after DMNL involve fibers entering or leaving the DMN from ventral and posterior directions, and they may be part of an opioid feeding system.

scholarly journals The Dorsomedial Hypothalamic Nucleus In Autonomic And Neuroendocrine Homeostasis

1975 ◽  
Vol 2 (1) ◽  
pp. 45-60 ◽  
Author(s):  
Lee L. Bernardis
Keyword(s):  
Growth Hormone ◽  
Electrical Stimulation ◽  
Food Intake ◽  
Present Report ◽  
Hypothalamic Nucleus ◽  
Control Mechanisms ◽  
Storage Site ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Cervical Stimulation ◽  
Stimulation Of

SUMMARY:Median eminence and ventromedial hypothalamus have in the past been the principal foci of research in neuroendocrine and neurovisceral control mechanisms. The present report provides an overview of work involving the dorsomedial hypothalamic nucleus (DMN). This structure is located dorsal to the ventromedial hypothalamic nucleus (VMN) and extends anteroposteriorly from the plane of the largest cross section of the VMN to the plane of the dorsal premammillary nucleus. Fibers from the DMN pass with the periventricular system and the dorsal longitudinal fasciculus of Schütz and have been traced to the midbrain tegmentum and reticular formation. Intrahypothalamic connections involve intensive networks between DMN, lateral hypothalamic nucleus (LHN) and VMN. Regarding neurotransmitters, recent studies indicate that the DMN receives noradrenergic innervation along two pathways, a dorsal and a ventral one. Monoamine-containing systems approach the DMN from the lateral hypothalamus and the bulk of these fibers are carried in the medium forebrain bundle from their cells of origin in the brain stem. Studies of the vascular supply indicate that both VMN and DMN receive their blood supply from the internal carotid artery. It has been recently demonstrated that the DMN is involved in the control of food intake and possibly water intake as well. Discrete lesions in the DMN have caused hypophagia and hypodipsia, and implantation of epinephrine and norepinephrine in this area has initiated eating. Many years ago, electrical stimulation of this area was reported to cause eating. Although DMN lesions cause hypodipsia, they do not result in the reduced water/food intake ratios that are so characteristic of the VMN syndrome. DMN lesions are also followed by reduced spontaneous activity (running wheel), but this reduced activity is not accompanied by increased weight gain and accretion of adipose tissue, the latter being consistently observed in the VMN rat. Rather, carcass fat remains normal in the DMN rat and carcass protein is either normal or slightly increased. Many of the aforementioned changes in weanling rats with DMN lesions, however, are not matched by similar alterations in the intermediary metabolism of carbohydrate and lipid. Possibly this is due to a “resetting” of a central autonomic control system that makes it possible for the DMN rat to adapt more efficiently to a reduced influx of substrate, i.e. the consistent hypophagia. From a review of the literature it appears that the DMN and their circuitry are involved in only a few neuroendocrine, i.e. hypothalamohypophyseal control mechanisms. Both lesion and cervical stimulation experiments suggest an involvement of the DMN in the control of LTH. Circumstantial evidence points to the DMN as a possible formation and/or storage site of growth hormone inhibiting factor (GIF). Although DMN rats show reduced ponderal and linear growth, they have been found to have normal or elevated plasma growth hormone (GH) levels. Both lesion and stimulation studies have yielded the impression that the DMN is not involved in thyroid, i.e., thyrotropin stimulating hormone releasing factor (TSHRF) control. Electrical stimulation of the DMN has been reported to result in a positive correlation between adrenal blood flow and adrenal corticoid release in hypophysectomized dogs. This has been interpreted as a coordinated response at the level of a “dorsomedial sympathetic vasodilator relay” rather than a “true” neuroendocrine effect via corticotropin releasing factor (CRF). Experiments that failed to demonstrate a relationship between the DMN and the tonic and cyclic control of luteinizing hormone releasing factor (LHRF) are discussed. The data reviewed indicate the existence in the dorsomedial hypothalamus of an area that exerts a profound influence on many aspects of neurovisceral and some neuroendocrine control systems.

Disturbances of growth hormone-insulin-like growth factor axis and response to growth hormone in acidosis

1998 ◽  
Vol 275 (1) ◽  
pp. R120-R128
Author(s):  
Karina Jandziszak ◽  
Carlos Suarez ◽  
Ethan Wasserman ◽  
Ross Clark ◽  
Bonnie Baker ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Linear Growth ◽  
Growth Failure ◽  
Serum Levels ◽  
Igf Binding Proteins ◽  
Gh Secretion ◽  
Term Administration ◽  
Igf Binding ◽  
Final Length

Severe chronic metabolic acidosis (CMA) in rats is associated with poor food intake and downregulation of growth hormone (GH), insulin-like growth factors (IGFs), and liver receptors; the administration of recombinant GH (rGH) fails to improve the growth failure. In mice with carbonic anhydrase II deficiency (CAD), a model of moderate CMA with food intake close to normal, we studied serum levels of GH, IGFs, and IGF-binding proteins, and the growth response to rGH. CAD was associated with low serum levels of GH in males. Randomized administration of rGH from ∼5 to ∼12 wk to CAD mice improved food efficiency and increased serum IGF-I levels, final length, and weight compared with placebo without affecting blood pH. Although administration of rGH also increased linear growth in healthy animals, the effect was less than that in CAD mice and was only observed when started before 6 wk of life. Thus growth failure in CAD mice is associated with a decrease in GH secretion in males but not in females. Long-term administration of rGH increases linear growth in CAD mice despite persistent CMA.

scholarly journals GLP-2 decreases food intake in the dorsomedial hypothalamic nucleus (DMH) through Exendin (9–39) in male Sprague-Dawley (SD) rats

2021 ◽  
Vol 229 ◽  
pp. 113253
Author(s):  
Huiling Sun ◽  
Kai Meng ◽  
Lin Hou ◽  
Lijun Shang ◽  
Jianqun Yan
Keyword(s):  
Food Intake ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Dorsomedial Hypothalamic Nucleus

scholarly journals Antiobesity Effects of the β-Cell Hormone Amylin in Diet-Induced Obese Rats: Effects on Food Intake, Body Weight, Composition, Energy Expenditure, and Gene Expression

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5855-5864 ◽  
Author(s):  
Jonathan D. Roth ◽  
Heather Hughes ◽  
Eric Kendall ◽  
Alain D. Baron ◽  
Christen M. Anderson
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Respiratory Quotient ◽  
Metabolic Effects ◽  
Mrna Levels ◽  
Lean Tissue ◽  
Reduced Body ◽  
Diet Induced Obesity ◽  
Cell Hormone

Effects of amylin and pair feeding (PF) on body weight and metabolic parameters were characterized in diet-induced obesity-prone rats. Peripherally administered rat amylin (300 μg/kg·d, 22d) reduced food intake and slowed weight gain: approximately 10% (P &lt; 0.05), similar to PF. Fat loss was 3-fold greater in amylin-treated rats vs. PF (P &lt; 0.05). Whereas PF decreased lean tissue (P &lt; 0.05 vs. vehicle controls; VEH), amylin did not. During wk 1, amylin and PF reduced 24-h respiratory quotient (mean ± se, 0.82 ± 0.0, 0.81 ± 0.0, respectively; P &lt; 0.05) similar to VEH (0.84 ± 0.01). Energy expenditure (EE mean ± se) tended to be reduced by PF (5.67 ± 0.1 kcal/h·kg) and maintained by amylin (5.86 ± 0.1 kcal/h·kg) relative to VEH (5.77 ± 0.0 kcal/h·kg). By wk 3, respiratory quotient no longer differed; however, EE increased with amylin treatment (5.74 ± 0.09 kcal/·kg; P &lt; 0.05) relative to VEH (5.49 ± 0.06) and PF (5.38 ± 0.07 kcal/h·kg). Differences in EE, attributed to differences in lean mass, argued against specific amylin-induced thermogenesis. Weight loss in amylin and pair-fed rats was accompanied by similar increases arcuate neuropeptide Y mRNA (P &lt; 0.05). Amylin treatment, but not PF, increased proopiomelanocortin mRNA levels (P &lt; 0.05 vs. VEH). In a rodent model of obesity, amylin reduced body weight and body fat, with relative preservation of lean tissue, through anorexigenic and specific metabolic effects.

Stimulation of food intake and weight gain in mature female rats by bovine prolactin and bovine growth hormone

1993 ◽  
Vol 264 (6) ◽  
pp. E986-E992 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
W. J. Salsgiver ◽  
J. G. Kostelc ◽  
R. J. Collier
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Mature Female ◽  
Female Rats ◽  
Bovine Growth Hormone ◽  
Female Rat ◽  
Moisture Percentage

Recombinant bovine prolactin (rbPRL) or bovine growth hormone (rbGH) was administered to mature female rats (10/treatment group) by daily subcutaneous injection for 10 days. Doses ranged from 7 to 5,000 micrograms/day (0.03-24 mg/kg body wt). Both rbPRL and rbGH increased body weight gain and food intake, but these parameters were increased at lower doses of rbPRL (7-63 micrograms/day) than rbGH (> 190 micrograms/day). Weight gain and food intake were maximally stimulated by 190 micrograms/day rbPRL, whereas maximal increased weight gain was obtained with the highest dose of rbGH (5,000 micrograms/day). Total carcass protein was increased by both hormones; however, protein as a percentage of body weight was unchanged. Similarly, neither rbPRL nor rbGH changed the percentage of carcass moisture. Percentage of body fat was increased by rbPRL but was decreased by rbGH. Weight of the gastrointestinal tract and kidneys was increased by both hormones, but increases were in proportion to body weight gain. These data confirm that ungulate prolactin is a hyperphagic agent in the female rat. In addition, they suggest that, while prolactin stimulates growth in mature female rats, this growth is probably not via a somatogenic mechanism.

Pulmonary delivery of peptide YY for food intake suppression and reduced body weight gain in rats

2011 ◽  
Vol 13 (5) ◽  
pp. 408-417 ◽  
Author(s):  
P. P. Nadkarni ◽  
R. M. Costanzo ◽  
M. Sakagami
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Peptide Yy ◽  
Body Weight Gain ◽  
Pulmonary Delivery ◽  
Reduced Body

Effects of hormones and hypoglycemic agents on testicular fat in the rat

1961 ◽  
Vol 200 (6) ◽  
pp. 1277-1284 ◽  
Author(s):  
T. C. Smith ◽  
L. Will ◽  
J. Oleson ◽  
K. -F. Benitz ◽  
J. Perrine ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Blood Glucose ◽  
Food Intake ◽  
Lipid Content ◽  
Fat Body ◽  
Hypoglycemic Agents ◽  
Hydrocortisone Acetate ◽  
Simultaneous Measurements ◽  
Fat Bodies

Response of transplanted and nontransplanted fat bodies to various hormones, tolbutamide, and hypoglycin A was compared by measuring the amount of lipids in the dissected fat bodies after 2 weeks treatment. Simultaneous measurements of food intake and body weight were made to serve as a basis for evaluating the effects on fat. Protamine zinc insulin produced an increase in lipid content of the testicular fat body, accompanied by elevation in food intake in three of five experiments; hydrocortisone acetate, triamcinolone or its 16,21-diacetate, or diethylstilbestrol brought about decreases in lipid with either no change or a decline in food intake; epinephrine·HCl or growth hormone elicited decreases in lipid without significantly influencing food intake or body weight. Generally, transplanted fat was more responsive to these agents than the undisturbed fat body. Both tolbutamide and hypoglycin A decreased lipids in the transplant without affecting those in untransplanted fat. Food intake, body weight, and blood glucose were not changed.

scholarly journals Development of obesity in transgenic rats with low circulating growth hormone levels: involvement of leptin resistance

2000 ◽  
pp. 535-541 ◽  
Author(s):  
Y Furuhata ◽  
R Kagaya ◽  
K Hirabayashi ◽  
A Ikeda ◽  
KT Chang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cerebrospinal Fluid ◽  
Body Weight ◽  
Weight Gain ◽  
Locomotor Activity ◽  
Food Intake ◽  
Body Weight Gain ◽  
Leptin Resistance ◽  
Intracerebroventricular Injection ◽  
Transgenic Rats

BACKGROUND: Human growth hormone (hGH) transgenic (TG) rats have been produced in our laboratory. These TG rats are characterized by low circulating hGH levels, virtually no endogenous rGH secretion, and massive obesity. OBJECTIVE: To elucidate how energy balance and leptin sensitivity contributed to the establishment of this obesity. DESIGN AND METHODS: Food intake, locomotor activity and leptin concentrations in serum and cerebrospinal fluid were measured in TG rats and their non-transgenic littermates (control). The effect of intraperitoneal and intracerebroventricular injection of leptin on food intake and body weight gain was also examined. RESULTS: An increase in food intake and a decrease in locomotor activity were observed from 4 and 7 weeks of age, respectively, in the transgenic rats compared with control. Serum leptin concentrations of the transgenic rats were more than twice as high as those of control rats and were associated with an increased white adipose tissue mass and ob gene expression. Intraperitoneal injection of leptin significantly decreased food intake and body weight gain in control rats, but not in transgenic rats. Leptin concentration in the cerebrospinal fluid of transgenic rats was not different from that of control rats, and intracerebroventricular injection of leptin was similarly effective in reducing food intake and body weight gain as it was in control rats. CONCLUSIONS: These results suggest that the transgenic rats, whose GH secretion is suppressed, develop obesity due to early onset of an increase in food intake and a decrease in locomotor activity with leptin resistance resulting from deteriorating leptin transport from peripheral blood to cerebrospinal fluid.

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