Effect of caloric restriction on body weight loss and body fat utilization in obese hyperglycemic mice (obob)

Metabolism ◽  
1972 ◽  
Vol 21 (1) ◽  
pp. 10-17 ◽  
Author(s):  
C. Chlouverakis
2005 ◽  
Vol 90 (8) ◽  
pp. 4659-4663 ◽  
Author(s):  
Petra Kok ◽  
Ferdinand Roelfsema ◽  
Janneke G. Langendonk ◽  
Marijke Frölich ◽  
Jacobus Burggraaf ◽  
...  

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5679-5687 ◽  
Author(s):  
James L. Trevaskis ◽  
Todd Coffey ◽  
Rebecca Cole ◽  
Chunli Lei ◽  
Carrie Wittmer ◽  
...  

Previously, we reported that combination treatment with rat amylin (100 μg/kg·d) and murine leptin (500 μg/kg·d) elicited greater inhibition of food intake and greater body weight loss in diet-induced obese rats than predicted by the sum of the monotherapy conditions, a finding consistent with amylin-induced restoration of leptin responsiveness. In the present study, a 3 × 4 factorial design was used to formally test for a synergistic interaction, using lower dose ranges of amylin (0, 10, and 50 μg/kg·d) and leptin (0, 5, 25, and 125 μg/kg·d), on food intake and body weight after 4 wk continuous infusion. Response surface methodology analysis revealed significant synergistic anorexigenic (P < 0.05) and body weight-lowering (P < 0.05) effects of amylin/leptin combination treatment, with up to 15% weight loss at doses considerably lower than previously reported. Pair-feeding (PF) experiments demonstrated that reduction of food intake was the predominant mechanism for amylin/leptin-mediated weight loss. However, fat loss was 2-fold greater in amylin/leptin-treated rats than PF controls. Furthermore, amylin/leptin-mediated weight loss was not accompanied by the counterregulatory decrease in energy expenditure and chronic shift toward carbohydrate (rather than fat) utilization observed with PF. Hepatic gene expression analyses revealed that 28 d treatment with amylin/leptin (but not PF) was associated with reduced expression of genes involved in hepatic lipogenesis (Scd1 and Fasn mRNA) and increased expression of genes involved in lipid utilization (Pck1 mRNA). We conclude that amylin/leptin interact synergistically to reduce body weight and adiposity in diet-induced obese rodents through a number of anorexigenic and metabolic effects.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Flavio Cadegiani ◽  
Pedro Luiz H da Silva

Abstract Background:Obesity is a chronic, multi-factorial, and relapsing disorder that has been reported to be a risk factor to more than 200 diseases, among which the majority is direct- or indirectly triggered by the metabolic abnormalities induced by excessive body fat. Indeed, patients with obesity tend to disclose multiple alterations of metabolic markers, which tend to improve with weight loss. Despite the multiple dysfunctions extensively in this population, only mandatory biochemical exams are usually ordered, likely due to limitations in cost and lack of cost-effectiveness, since the majority of the parameters typically altered in obesity does not drive therapeutic choices or influence in an individual-based evaluation.We developed a protocol for obesity treatment that includes a thorough analysis and follow up of the biochemical parameters of patients with obesity, including more than 50 parameters, for more precise diagnosis and response to treatments. Among these parameters, we identified unexpected changes, including some that would initially be related to increased cardiovascular risk or worse prognosis when in an usual context, but which could peculiarly indicate successfulness of weight loss, since these parameters tend to return to normal levels after a period in the new body weight. Our objective is to identify whether these paradoxical changes in biomarkers are linearly correlated with body weight loss, fat loss, mass loss, or whether they were related to the use of any anti-obesity drug. Methods: In a retrospective cohort of 1,567 patients that underwent a clinical weight loss treatment for obesity in a obesity center (Corpometria Institute, Brasília, DF, Brazil), we performed a linear association analysis between body weight and body fat (air displacement pletismography - Bod Pod, CosMed, USA) and 65 parameters, including hormonal, metabolic, inflammatory, and immunologic parameters. We also adjusted for the use of anti-obesity drugs. Results: Homocysteine and triglycerides were identified to increase linearly according to the amount of weight loss (r = -0.77) and fat loss (r = -0.85), but not due to the use of any drug. Folic acid decrease was directly related to fat loss (r = 0.81). Additional findings include more significant decrease of ApoB, compared to LDLc, decreases of GGT, ALT, CRP, ESR, neutrophils, ferritin, fibrinogen, PTH, free T3, uric acid, a and temporary decrease of ApoA and HDLc, all related with body fat loss. Conclusions: Increase of homocysteine resulted from decreased folic acid metabolism, and increased triglycerides may be indirect markers of lipolysis, as no other plausible mechanism could explain these findings.


1968 ◽  
Vol 46 (1) ◽  
pp. 101-107
Author(s):  
Peter B. Karch ◽  
John R. Beaton

With adult male rats, experiments were carried out to ascertain the different effects, if any, of isocaloric diets high in carbohydrate, fat, or protein fed in restricted amounts of 9 g per rat per day on body weight loss and composition. It was observed that the nature of the diet did not alter rate, amount, or composition of body weight loss when fed in restricted amount for a period of 12 days. Further, the nature of the diet did not alter significantly the following parameters during restriction: water intake, urine volume, resting metabolic rate, spontaneous activity, urine and feces calorie values. In an experiment with hypothalamic-obese rats, the body weight loss and composition were not significantly different among the dietary-restricted groups. An important observation in this experiment was that as body fat decreased markedly owing to restricted feeding, body water increased markedly and counterbalanced approximately 60% of the potential weight loss due to the decrease in body fat. Our reported observations do not support the hypothesis that the composition of the diet may determine the rate and amount of body weight loss as a consequence of restricted food intake. They do support the hypothesis that the calorie intake, not the nature of the source of calories, determines the rate and amount of weight loss, at least for relatively short periods of food restriction.


2006 ◽  
Vol 52 (6) ◽  
pp. 672-683 ◽  
Author(s):  
Yuji Tominaga ◽  
Tatsumasa Mae ◽  
Mitsuaki Kitano ◽  
Yoshiro Sakamoto ◽  
Hideyuki Ikematsu ◽  
...  

1964 ◽  
Vol 19 (5) ◽  
pp. 863-867 ◽  
Author(s):  
Arthur M. Kodama ◽  
Nello Pace

Body fat content and the melting point and fatty acid composition of body fat of hamsters exposed to 35, 27, 20, 15, 10, and 6 C for 2 weeks were determined. The relationship between exposure temperature and body fat content and composition resembled that between environmental temperature and metabolic rate. Below the critical temperature, there was a progressive decrease in total body fat content and melting point accompanied by a decrease in the mole fraction of palmitic acid and an increase in the mole fraction of oleic acid. The softening of body fat in cold-exposed animals appears to be the result of an increased mobilization of depot fat in response to a higher metabolic rate in the cold, a mobilization which is at least partially selective with respect to individual fatty acids or triglycerides. Examination of changes in whole body composition revealed that 72% of the loss in body weight of hamsters exposed to 6 C was due to a decrease in body fat content. In contrast, the decrease in body fat content accounted for only 28% of the body weight loss of pair-fed hamsters kept at 27 C on reduced caloric intake to match the body weight loss experienced by cold-exposed animals. It appears, therefore, that cold exposure induces a more effective fat depot mobilization than does reduced caloric intake. heat exposure; cold exposure; body composition Submitted on February 3, 1964


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1965-P
Author(s):  
TEAYOUN KIM ◽  
JESSICA P. ANTIPENKO ◽  
SHELLY NASON ◽  
NATALIE PRESEDO ◽  
WILLIAM J. VAN DER POL ◽  
...  

2018 ◽  
Vol 44 (1) ◽  
Author(s):  
Ayako Ito ◽  
Aya Nozaki ◽  
Ichiro Horie ◽  
Takao Ando ◽  
Atsushi Kawakami

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