Obesity from eating elicited by daily stimulation of hypothalamus

1965 ◽  
Vol 208 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Eric A. Steinbaum ◽  
Neal E. Miller
Keyword(s):  
Electrical Stimulation ◽  
Weight Gain ◽  
Lateral Hypothalamus ◽  
High Fat Diet ◽  
Daily Intake ◽  
High Fat ◽  
Total Daily Intake ◽  
Short Time ◽  
Normal Daily Intake ◽  
Stimulation Of

Rats who were forced to overeat wet mash by electrical stimulation of the lateral hypothalamus 2 hr/day for 31 days became obese by maintaining an intake and rate of weight gain far greater than nonstimulated animals or animals similarly stimulated without food present. The rats stimulated without food present gained less weight over the 31-day period, ate less in the hour after each stimulation, but were not significantly different from the nonstimulated rats in total daily intake. In a second experiment, using a high-fat diet instead of wet mash, rats stimulated to eat varying fractions (0, 33, 66, 100%) of their normal daily intake in a short time each day were found abruptly to reduce their intake the rest of the day so that total daily intake remained normal.

Diminished cardiovascular responsiveness to vagal stimulation in obese rats

1990 ◽  
Vol 259 (4) ◽  
pp. R842-R848 ◽  
Author(s):  
R. D. Bunag ◽  
D. Krizsan ◽  
H. Itoh
Keyword(s):  
Electrical Stimulation ◽  
High Fat Diet ◽  
Plasma Insulin ◽  
Vagal Stimulation ◽  
High Fat ◽  
Borderline Hypertension ◽  
Reflex Bradycardia ◽  
Obese Rats ◽  
Tail Cuff ◽  
Stimulation Of

Obese rats maintained on a high-fat diet since weaning were studied to determine whether parasympathetic deficiencies contribute to the cardiovascular malfunction in obesity. Elevations in tail-cuff systolic pressures and plasma insulin indicated that obese rats had borderline hypertension and hyperinsulinemia. Reflex bradycardia produced by angiotensin or phenylephrine in conscious obese rats was less than that in age-matched controls. However, reflex responses elicited by phenylephrine or sodium nitroprusside when the same rats were later anesthetized did not differ between groups. Impairment of afferent or central components of the baroreflex arc was considered unlikely, because depressor, bradycardic, and sympathoinhibitory responses to electrical stimulation of aortic depressor afferents were similar in both rat groups. By contrast, efferent parasympathetic mediation was probably reduced, since depressor and bradycardic responses to electrical stimulation of vagal nerve efferents were significantly smaller in obese than in control rats. Collectively our findings suggest that cardiovascular and baroreflex malfunction in obese rats may result from an autonomic imbalance involving diminished parasympathetic activity.

scholarly journals Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice

2021 ◽  
Vol 22 (10) ◽  
pp. 5390
Author(s):  
Qianhui Zeng ◽  
Nannan Wang ◽  
Yaru Zhang ◽  
Yuxuan Yang ◽  
Shuangshuang Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Chow Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Partial Deficiency

Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217+/− mice had less weight gain than Zfp217+/+ mice. Histological observations revealed that Zfp217+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217+/+ mice compared to Zfp217+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity.

Acute electrical stimulation of lateral hypothalamus increases natural killer cell activity in rats

1996 ◽  
Vol 67 (1) ◽  
pp. 67-70 ◽  
Author(s):  
Marcus Wenner ◽  
Noriyuki Kawamura ◽  
Hitoshi Miyazawa ◽  
Yukihiro Ago ◽  
Toshio Ishikawa ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Lateral Hypothalamus ◽  
Natural Killer Cell Activity ◽  
Killer Cell ◽  
Cell Activity ◽  
Killer Cell Activity ◽  
Stimulation Of

Stimulation of fecal fat excretion and the disposal of protoporphyrin in a murine model for erythropoietic protoporphyria

2007 ◽  
Vol 293 (2) ◽  
pp. G510-G516
Author(s):  
Karin E. R. Gooijert ◽  
Rick Havinga ◽  
Alida R. Oosterloo-Duinkerken ◽  
Enge E. A. Venekamp-Hoolsema ◽  
Folkert Kuipers ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fecal Excretion ◽  
High Fat ◽  
Erythropoietic Protoporphyria ◽  
Low Fat Diet ◽  
Fecal Fat ◽  
Sucrose Polyesters ◽  
Hydrophobic Compound ◽  
Fat Excretion ◽  
Stimulation Of

Erythropoietic protoporphyria (EPP) is characterized by toxic accumulation of the hydrophobic compound protoporphyrin (PP). Ferrochelatase-deficient ( fch/ fch) mice are an animal model for human EPP. Recently, we have demonstrated that the accumulation of another hydrophobic compound, unconjugated bilirubin, could effectively be treated by stimulation of fecal fat excretion. We investigated whether stimulation of fecal fat excretion enhanced the disposal of PP in fch/ fch mice. Fch/ fch mice were fed for 8 wk with a high-fat diet (16 wt% fat; control) or with the high-fat diet mixed with either a nonabsorbable fat (sucrose polyester) or the intestinal lipase inhibitor orlistat. The effects of the treatments on fecal excretion of fat and PP and on hepatic PP concentrations were compared with control diets. Fecal fat excretion in fch/ fch mice on a high-fat diet was higher than in mice on a low-fat diet (+149%, P < 0.05). Sucrose polyesters and orlistat increased fecal fat excretion even more, up to sixfold of control values. However, none of the different treatments affected fecal PP excretion or hepatic PP concentration. Treatment of fch/ fch mice with a high-fat diet, a nonabsorbable fat diet, or with orlistat increased the fecal excretion of fat but did not increase fecal PP excretion or decrease hepatic PP concentration. The present data indicate that accumulation of PP is not amenable to stimulation of fecal fat excretion.

scholarly journals ApoE Gene Deficiency Enhances the Reduction of Bone Formation Induced by a High-Fat Diet Through the Stimulation of p53-Mediated Apoptosis in Osteoblastic Cells

2007 ◽  
Vol 22 (7) ◽  
pp. 1020-1030 ◽  
Author(s):  
Hideyuki Hirasawa ◽  
Shinya Tanaka ◽  
Akinori Sakai ◽  
Masato Tsutsui ◽  
Hiroaki Shimokawa ◽  
...  
Keyword(s):  
Bone Formation ◽  
High Fat Diet ◽  
Apoe Gene ◽  
Osteoblastic Cells ◽  
High Fat ◽  
Gene Deficiency ◽  
Stimulation Of

Adrenergic Stimulation of the Rat Diencephalon and its Effect on Food Intake and Hoarding Activity

1970 ◽  
Vol 22 (2) ◽  
pp. 125-132 ◽  
Author(s):  
J. E. Blundell ◽  
L. J. Herberg
Keyword(s):  
Electrical Stimulation ◽  
Food Intake ◽  
Food Deprivation ◽  
Lateral Hypothalamus ◽  
Adrenergic Stimulation ◽  
Feeding Mechanism ◽  
Stimulation Of ◽  
Nutritional Depletion

The diencephalic area most sensitive to microinjections of noradrenaline lay outside the area of the lateral hypothalamus in which feeding can be produced by electrical stimulation. Injection of either area, including injections that caused increased feeding, failed to have any effect on hoarding activity. Since hoarding can be elicited both by food deprivation and by electrical stimulation of the lateral hypothalamus, these findings indicate biochemical, anatomical and motivational differences between the central feeding mechanism sensitive to adrenergic stimulation, and that responding to electrical stimulation or nutritional depletion. The former mechanism may be disinhibitory; the latter, excitatory.

Sign in / Sign up

Export Citation Format

Share Document