Energy balance and regulation of body weight after intestinal bypass surgery in rats

1983 ◽  
Vol 245 (5) ◽  
pp. R658-R663 ◽  
Author(s):  
R. L. Atkinson ◽  
E. L. Brent ◽  
B. S. Wagner ◽  
J. H. Whipple
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Bypass Surgery ◽  
Calorie Intake ◽  
Intestinal Bypass ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Body Weights

This study evaluated the possibility that intestinal bypass surgery alters energy balance and regulation of body weight. In two sets of experiments, male Sprague-Dawley rats underwent bypass or sham bypass surgery. In experiment 1, half of each group was overfed and half was underfed. Bypass reduced net calorie intake (intake - fecal loss) at 2 wk but not at 6 wk. Body weights were maintained at a much lower level in the bypass rats, yet apparent energy expenditure was greater. In experiment 2, bypass rats were compared with sham bypass and sham bypass who were food restricted for paired-weight-loss to bypass (PWL sham). Net calorie intake and body weights of bypass and sham bypass followed a similar pattern as in experiment 1. At similar levels of body weight postoperatively, bypass rats required more calories per kilogram than did the PWL shams, suggesting that bypass resets downward the level at which body weight is regulated. Calorie requirements correlated with food intake better than with absolute body weight. Further studies to determine the mechanism of altered energy expenditure may provide methods for weight loss without extensive surgery.

Appetite suppressant activity in plasma of rats after intestinal bypass surgery

1982 ◽  
Vol 243 (1) ◽  
pp. R60-R64 ◽  
Author(s):  
R. L. Atkinson ◽  
E. L. Brent
Keyword(s):  
Food Intake ◽  
Polymorphonuclear Leukocytes ◽  
Bypass Surgery ◽  
Aversive Conditioning ◽  
Jejunoileal Bypass ◽  
Intestinal Bypass ◽  
Sprague Dawley ◽  
Appetite Suppressant ◽  
Sprague Dawley Rats ◽  
Subsequent Intake

Male Sprague-Dawley rats with a jejunoileal bypass ate 32% less in the 1st h of refeeding after an overnight fast than did sham-bypass rats. Fasted recipients injected intraperitoneally with 6-7 ml of bypass plasma also ate 32% less (P less than 0.001) during the 1st h of refeeding than did recipients of sham-bypass plasma, but subsequent intake was not significantly different. Rectal temperature, hematocrit, white blood cell count, and percent polymorphonuclear leukocytes were not different between bypass and sham-bypass rats. A test for aversive conditioning suggested that the effect of bypass plasma was not due to illness or discomfort. These data suggest that intestinal bypass produces a transferable humoral factor that suppresses food intake and that the effect is not due to illness or discomfort. If the decreased food intake in humans after intestinal bypass is due to a similar mechanism, the possibility exists that this humoral appetite-suppressant factor may be clinically useful in the treatment of morbid obesity.

Energy balance of rats with lateral hypothalamic lesions

1982 ◽  
Vol 242 (4) ◽  
pp. E273-E279 ◽  
Author(s):  
S. W. Corbett ◽  
R. E. Keesey
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Caloric Intake ◽  
Energy Utilization ◽  
Lateral Hypothalamic ◽  
Energy Needs ◽  
Body Weights ◽  
Maintain Body Weight

Rats with lateral hypothalamic (LH) lesions maintain body weight at a chronically reduced percentage of nonlesioned controls. An assessment of how they achieve energy balance at subnormal weight levels entailed a determination of both their energy intake and their energy expended or lost in processing ingested food, on basal heat production, on activity, and in feces or urine. It was found that the caloric intake and expenditure of LH-lesioned animals, though significantly lower than those of controls, were appropriate to the reduced metabolic body size (BW0.75) that they maintained. Likewise, energy expenditure in the LH-lesioned animals was normal in that the proportion of their ingested energy relegated to 1) basal metabolism, 2) the processing food, and 3) activity was the same as that of nonlesioned controls. Thus, unlike nonlesioned rats, which at lowered body weights both decrease their energy needs and reorder the pattern of energy expenditure, LH-lesioned animals display a normal pattern of energy utilization at reduced weight levels. These findings provide further evidence that lateral hypothalamic mechanisms play an important role in setting the level at which body weight is regulated.

scholarly journals Central Sirt1 Regulates Body Weight and Energy Expenditure Along With the POMC-Derived Peptide α-MSH and the Processing Enzyme CPE Production in Diet-Induced Obese Male Rats

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 961-974 ◽  
Author(s):  
Nicole E. Cyr ◽  
Jennifer S. Steger ◽  
Anika M. Toorie ◽  
Jonathan Z. Yang ◽  
Ronald Stuart ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Obese Individual ◽  
Nutrient Sensing ◽  
Sirtuin 1 ◽  
Male Rats ◽  
Sprague Dawley ◽  
Phosphorylated Akt ◽  
Central Inhibition

Abstract In the periphery, the nutrient-sensing enzyme Sirtuin 1 (silent mating type information regulation 2 homolog 1 [Sirt1]) reduces body weight in diet-induced obese (DIO) rodents. However, the role of hypothalamic Sirt1 in body weight and energy balance regulation is debated. The first studies to reveal that central Sirt1 regulates body weight came from experiments in our laboratory using Sprague-Dawley rats. Central inhibition of Sirt1 decreased body weight and food intake as a result of a forkhead box protein O1 (FoxO1)-mediated increase in the anorexigenic proopiomelanocortin (POMC) and decrease in the orexigenic Agouti-related peptide in the hypothalamic arcuate nucleus. Here, we demonstrate that central inhibition of Sirt1 in DIO decreased body weight and increased energy expenditure at higher levels as compared with the lean counterpart. Brain Sirt1 inhibition in DIO increased acetylated FoxO1, which in turn increased phosphorylated FoxO1 via improved insulin/phosphorylated AKT signaling. Elevated acetylated FoxO1 and phosphorylated FoxO1 increased POMC along with the α-melanocyte-stimulating hormone (α-MSH) maturation enzyme carboxypeptidase E, which resulted in more of the bioactive POMC product α-MSH released into the paraventricular nucleus. Increased in α-MSH led to augmented TRH levels and circulating T3 levels (triiodothyronine, thyroid hormone). These results indicate that inhibiting hypothalamic Sirt1 in DIO enhances the activity of the hypothalamic-pituitary-thyroid axis, which stimulates energy expenditure. Because we show that blocking central Sirt1 causes physiological changes that promote a negative energy balance in an obese individual, our results support brain Sirt1 as a significant target for weight loss therapeutics.

scholarly journals Increasing Energy Flux to Maintain Diet-Induced Weight Loss

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2533 ◽  
Author(s):  
Christopher L. Melby ◽  
Hunter L. Paris ◽  
R. Drew Sayer ◽  
Christopher Bell ◽  
James O. Hill
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Energy Flux ◽  
Weight Maintenance ◽  
High Energy ◽  
Daily Energy

Long-term maintenance of weight loss requires sustained energy balance at the reduced body weight. This could be attained by coupling low total daily energy intake (TDEI) with low total daily energy expenditure (TDEE; low energy flux), or by pairing high TDEI with high TDEE (high energy flux). Within an environment characterized by high energy dense food and a lack of need for movement, it may be particularly difficult for weight-reduced individuals to maintain energy balance in a low flux state. Most of these individuals will increase body mass due to an inability to sustain the necessary level of food restriction. This increase in TDEI may lead to the re-establishment of high energy flux at or near the original body weight. We propose that following weight loss, increasing physical activity can effectively re-establish a state of high energy flux without significant weight regain. Although the effect of extremely high levels of physical activity on TDEE may be constrained by compensatory reductions in non-activity energy expenditure, moderate increases following weight loss may elevate energy flux and encourage physiological adaptations favorable to weight loss maintenance, including better appetite regulation. It may be time to recognize that few individuals are able to re-establish energy balance at a lower body weight without permanent increases in physical activity. Accordingly, there is an urgent need for more research to better understand the role of energy flux in long-term weight maintenance.

Prevention of stress-induced weight loss by third ventricle CRF receptor antagonist

1999 ◽  
Vol 276 (5) ◽  
pp. R1461-R1468 ◽  
Author(s):  
Gennady N. Smagin ◽  
Leigh Anne Howell ◽  
Stephen Redmann ◽  
Donna H. Ryan ◽  
Ruth B. S. Harris
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Receptor Antagonist ◽  
Acute Stress ◽  
Third Ventricle ◽  
Corticotropin Releasing Factor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sustained Reduction ◽  
Acute Responses

We previously reported that rats exposed to repeated restraint (3 h/day for 3 days) experience temporary hypophagia and a sustained reduction in body weight compared with nonrestrained controls. Studies described here determined the involvement of central corticotropin-releasing factor (CRF) receptors in the initiation of this chronic response to acute stress. In experiment 1, Sprague-Dawley rats were fitted with cannulas in the lateral ventricle and infused with 50 μg of αhCRF-(9—41) or saline immediately before restraint on each of the 3 days of restraint. The receptor antagonist inhibited hypophagia and weight loss on day 1 of restraint but not on days 2 and 3. In experiment 2, 10 μg of αhCRF-(9—41) or saline were infused into the third ventricle immediately before each restraint. The receptor antagonist totally blocked stress-induced hypophagia and weight loss. These results demonstrate that CRF receptors located in or near the hypothalamus mediate the acute responses to stress that lead to a permanent change in the hormonal or metabolic processes that determine body weight and body composition.

scholarly journals Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesity

2002 ◽  
Vol 282 (1) ◽  
pp. R46-R54 ◽  
Author(s):  
Barry E. Levin ◽  
Ambrose A. Dunn-Meynell
Keyword(s):  
Body Weight ◽  
Energy Content ◽  
Selective Reduction ◽  
High Energy ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Diet Induced Obesity ◽  
Background Diet ◽  
Sprague Dawley Rats ◽  
Body Weights

Sprague-Dawley rats selectively bred for diet-induced obesity (DIO) or diet resistance (DR) were characterized on diets of differing energy content and palatability. Over 10 wk, DR rats on a high-energy (HE) diet (31% fat) gained weight similarly to DR rats fed chow (4.5% fat), but they became obese on a palatable liquid diet (Ensure). DIO rats gained 22% more weight on an HE diet and 50% more on Ensure than chow-fed DIO rats. DIO body weight gains plateaued when switched from HE diet to chow. But, Ensure-fed DIO rats switched to chow spontaneously reduced their intake and weight to that of rats switched from HE diet to chow. They also reduced their hypothalamic proopiomelanocortin and dynorphin but not neuropeptide Y mRNA expression by 17–40%. When reexposed to Ensure after 7 wk, they again overate and matched their body weights to rats maintained on Ensure throughout. All Ensure-fed rats had a selective reduction in dynorphin mRNA in the ventromedial hypothalamic nucleus. Thus genetic background, diet composition, and palatability interact to produce disparate levels of defended body weight and central neuropeptide expression.

scholarly journals Dietary Exposure to Oxidized Frying Oil from Fetus to Adulthood Suppresses Male Reproductive Development by Altering Testicular Cholesterol and Testosterone Homeostasis in Sprague Dawley Rats

2020 ◽  
Vol 150 (7) ◽  
pp. 1713-1721
Author(s):  
Hai-Ping Wu ◽  
Yu-Shun Lin ◽  
Chi-Fen Chang ◽  
Shui-Yuan Lu ◽  
Pei-Min Chao
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Soybean Oil ◽  
Body Weight Loss ◽  
Reproductive Development ◽  
Frying Oil ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

ABSTRACT Background Dietary frying oil may have endocrine-disrupting effects, as a feminization effect was observed in cohorts of C57BL/6J male mice fetuses from dams consuming oxidized frying oil (OFO) during pregnancy. Objective The aim of present study was to test the hypothesis that OFO is an anti-androgen. Methods In experiment 1, male progeny of Sprague Dawley female rats fed fresh oil or an OFO diet (10 g fat/100 g, from fresh or 24-h–fried soybean oil; [control diet (C) and OFO groups, respectively] from midgestation through lactation were studied. Pups were weaned at 3 wk of age and then consumed their mothers’ diet until 9 wk of age. In addition, a group of dams and pups that consumed a high-fat diet (HF; 10 g fried and 20 g fresh soybean oil/100 g) was included to counteract body-weight loss associated with OFO ingestion. Indices of male reproductive development and testosterone homeostasis were measured. In experiment 2, male rats were allocated to C and OFO groups (treated as above) and indices of male fertility compared at 9–10 wk of age. Results In experiment 1, final body weights of the HF group were lower (17%) than the C group but higher (14%) than the OFO group (P < 0.0001 for each). In addition to abnormalities in seminiferous tubules, HF and OFO groups did not differ from one another, but, compared with the C group, had delayed preputial separation (4.9 d) and reductions in serum testosterone concentrations (17–74%), anogenital distance (8–20%), weights of androgen-dependent tissues (8–30%), testicular testosterone and cholesterol concentrations (30–40%), and mRNA levels of genes involved in steroidogenesis and cholesterol homeostasis (30–70%). In experiment 2, OFO-exposed males had 20% lower sperm motility (P < 0.05); however, when mated to normal females, pregnancy rates and litter sizes did not differ between OFO and C groups. Conclusions The anti-androgenic effect of OFO in Sprague Dawley rats was attributed to decreased testicular concentrations of cholesterol (testosterone precursor) and not body-weight loss.

scholarly journals Kisspeptin antagonist prevents RF9-induced reproductive changes in female rats

Reproduction ◽  
2015 ◽  
Vol 149 (5) ◽  
pp. 465-473 ◽  
Author(s):  
Zafer Sahin ◽  
Sinan Canpolat ◽  
Mete Ozcan ◽  
Tuba Ozgocer ◽  
Haluk Kelestimur
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Female Rats ◽  
Central Administration ◽  
Vaginal Opening ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Induced Changes ◽  
Lh Secretion

The aim of this study was to determine the modulatory effects of peptide 234 (p234) (an antagonist of GPR54 receptors) on kisspeptin and RF9 (an RFamide-related peptide antagonist)-induced changes in reproductive functions and energy balance in female rats. Female Sprague–Dawley rats were weaned on postnatal day (pnd) 21. The animals were intracerebroventricularly cannulated under general anesthesia on pnd 23. Groups of female rats were injected with kisspeptin, RF9, p234, kisspeptin plus p234, or RF9 plus p234, daily. The experiments were ended on the day of first diestrus following pnd 60. Kisspeptin or RF9 alone advanced vaginal opening (VO), which was delayed by administration of kisspeptin antagonist alone. In the rats given kisspeptin plus p234 or RF9 plus p234, VO was not different from control rats. Kisspeptin and RF9 elicited significant elevations in circulating LH levels. Coadministrations of kisspeptin or RF9 with p234 decreased LH levels significantly. The use of p234 alone did not cause any significant change in LH secretion. Kisspeptin decreased both food intake and body weight while RF9 decreased only food intake without affecting body weight. The effects of kisspeptin on energy balance were also reversed by central administration of p234. In conclusion, kisspeptin antagonist, p234, modulates the effects of kisspeptin on reproductive functions and energy balance, whereas RF9 seems to exert only its effects on reproductive functions by means of GPR54 signaling in female rats.

scholarly journals Effect of DDT exposure on lipids and energy balance in obese Sprague-Dawley rats before and after weight loss

2015 ◽  
Vol 2 ◽  
pp. 990-995 ◽  
Author(s):  
Tomoko Ishikawa ◽  
James L. Graham ◽  
Kimber L. Stanhope ◽  
Peter J. Havel ◽  
Michele A. La Merrill
Keyword(s):  
Weight Loss ◽  
Energy Balance ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Before And After

Tumor-Promoting, Initiating, and Hepatotoxic Effects of 3,4,3',4'-Tetrabromobiphenyl (34-TBB) in Rats

1988 ◽  
Vol 7 (5) ◽  
pp. 687-697 ◽  
Author(s):  
D. Dixon ◽  
S.D. Sleight ◽  
S.D. Aust ◽  
M.S. Rezabek
Keyword(s):  
Body Weight ◽  
Tumor Promotion ◽  
Ultrastructural Changes ◽  
Hepatic Enzyme ◽  
Sprague Dawley ◽  
Gamma Glutamyl Transpeptidase ◽  
Sprague Dawley Rats ◽  
Body Weights ◽  
Tissue Changes ◽  
Glutamyl Transpeptidase

Female, 180–200 g Sprague-Dawley rats were used to determine if 3,4,3',4'-tetrabromobi-phenyl (34-TBB) is a promoter or initiator in a two-stage hepatocarcinogenesis assay. To test for promotion, rats were partially hepatectomized (PH) 24 hr before initiation (day 1) with 10 mg of diethylnitrosamine (DEN)/kg body weight given intraperitoneally (IP). Thirty days later, promotion was with 34-TBB (0.1,1 or 5 mg/kg) or phenobarbital (PB) (500 mg/kg) in diets for 180 days. To test for initiation, rats were PH and were initiated on day 1 with 34-TBB (1, 5, or 10 mg/kg) orally or DEN (10 mg/kg) IP. On day 31, promotion was with 500 mg of PB/kg of diet for 180 days. Noninitiated and non-PH rats were used to assess the histological and ultrastructural tissue changes associated with administration of 34-TBB in the diet for 180 days. Tumor promotion-initiation were assessed by counting and measuring hepatic enzyme-altered foci (EAF) with gamma-glutamyl transpeptidase (GGT) activity. Congener 34-TBB acts as a promoter in experimental hepatocarcinogenesis in rats, as evidenced by increased numbers of GGT-positive EAF. Also, 34-TBB may have initiation potential, as suggested by increased numbers of EAF in rats initiated with 34-TBB and promoted by PB. Dietary administration of 34-TBB for 180 days is not severely toxic in rats, as evidenced by mild histological and ultrastructural changes and minimal alterations in organ and body weights. Congener 34-TBB does not accumulate in liver and adipose tissue of rats.

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