Effects of high fat diets on caloric intake body weight, and heat-escape responses in normal and hyperphagic rats.

1969 ◽  
Vol 68 (4) ◽  
pp. 507-515 ◽  
Author(s):  
James M. Lipton
Keyword(s):  
Body Weight ◽  
Caloric Intake ◽  
High Fat ◽  
High Fat Diets ◽  
Escape Responses ◽  
Fat Diets

Effects of high-fat diets with different carbohydrate-to-protein ratios on energy homeostasis in rats with impaired brain melanocortin receptor activity

2005 ◽  
Vol 289 (1) ◽  
pp. R156-R163 ◽  
Author(s):  
C. Morens ◽  
M. Keijzer ◽  
K. de Vries ◽  
A. Scheurink ◽  
G. van Dijk
Keyword(s):  
Body Weight ◽  
Energy Homeostasis ◽  
Caloric Intake ◽  
Melanocortin Receptor ◽  
High Fat ◽  
Macronutrient Composition ◽  
Plasma Adiponectin ◽  
High Fat Diets ◽  
Glucose Tolerant ◽  
Fat Diets

Changes in dietary macronutrient composition and/or central nervous system neuronal activity can underlie obesity and disturbed fuel homeostasis. We examined whether switching rats from a diet with high carbohydrate content (HC; i.e., regular chow) to diets with either high fat (HF) or high fat/high protein content at the expense of carbohydrates (LC-HF-HP) causes differential effects on body weight and glucose homeostasis that depend on the integrity of brain melanocortin (MC) signaling. In vehicle-treated rats, switching from HC to either HF or LC-HF-HP feeding caused similar reductions in food intake without alterations in body weight. A reduced caloric intake (−16% in HF and LC-HF-HP groups) required to maintain or increase body weight underlay these effects. Chronic third cerebroventricular infusion of the MC receptor antagonist SHU9119 (0.5 nmol/day) produced obesity and hyperphagia with an increased food efficiency again observed during HF (+19%) and LC-HF-HP (+33%) feeding. In this case, however, HF feeding exaggerated SHU9119-induced hyperphagia and weight gain relative to HC and LC-HF-HP feeding. Relative to vehicle-treated controls, SHU9119 treatment increased plasma insulin (2.8–4 fold), leptin (7.7–15 fold), and adiponectin levels (2.4–3.7 fold), but diet effects were only observed on plasma adiponectin (HC and LC-HF-HP<HF). Finally, SHU9119-treated LC-HF-HP-fed rats were less glucose tolerant than others. Relatively low plasma adiponectin levels likely contributed to this effect. Thus HF feeding amplifies obesity induced by impaired MC signaling, provided that the carbohydrate-to-protein (C/P) ratio is high enough. Reduction of the C/P ratio within a HF diet ameliorates hyperphagia and obesity in rats with impaired MC signaling but aggravates associated disturbances in fuel homeostasis.

Eisenia bicyclis Inhibits Body Weight Gain and Fat Accumulation Induced by High-Fat Diets in Mice

2010 ◽  
Vol 15 (4) ◽  
pp. 262-266 ◽  
Author(s):  
Won-Hee Choi ◽  
Ji-Yun Ahn ◽  
Sun-A Kim ◽  
Tae-Wan Kim ◽  
Tae-Youl Ha
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
High Fat ◽  
Eisenia Bicyclis ◽  
Fat Accumulation ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals Adult offspring of high-fat diet-fed dams can have normal glucose tolerance and body composition

2014 ◽  
Vol 5 (3) ◽  
pp. 229-239 ◽  
Author(s):  
K. M. Platt ◽  
R. J. Charnigo ◽  
K. J. Pearson
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
High Fat ◽  
High Fat Diets ◽  
Normal Glucose ◽  
Fat Diets

Maternal high-fat diet consumption and obesity have been shown to program long-term obesity and lead to impaired glucose tolerance in offspring. Many rodent studies, however, use non-purified, cereal-based diets as the control for purified high-fat diets. In this study, primiparous ICR mice were fed purified control diet (10–11 kcal% from fat of lard or butter origin) and lard (45 or 60 kcal% fat) or butter (32 or 60 kcal% fat)-based high-fat diets for 4 weeks before mating, throughout pregnancy, and for 2 weeks of nursing. Before mating, female mice fed the 32 and 60% butter-based high-fat diets exhibited impaired glucose tolerance but those females fed the lard-based diets showed normal glucose disposal following a glucose challenge. High-fat diet consumption by female mice of all groups decreased lean to fat mass ratios during the 4th week of diet treatment compared with those mice consuming the 10–11% fat diets. All females were bred to male mice and pregnancy and offspring outcomes were monitored. The body weight of pups born to 45% lard-fed dams was significantly increased before weaning, but only female offspring born to 32% butter-fed dams exhibited long-term body weight increases. Offspring glucose tolerance and body composition were measured for at least 1 year. Minimal, if any, differences were observed in the offspring parameters. These results suggest that many variables should be considered when designing future high-fat diet feeding and maternal obesity studies in mice.

Effect of nutrition on growth and somatomedin A levels in the rat

1980 ◽  
Vol 94 (3) ◽  
pp. 321-326 ◽  
Author(s):  
Kazue Takano ◽  
Naomi Hizuka ◽  
Kazuo Shizume ◽  
Yoko Hasumi ◽  
Toshio Tsushima
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Normal Growth ◽  
Protein Diet ◽  
Low Protein Diet ◽  
High Fat ◽  
Low Protein ◽  
High Fat Diets ◽  
Hypophysectomized Rats ◽  
Fat Diets

Abstract. Serum somatomedin A was significantly reduced after 3 days of fasting in rats with a mean decrease of 23.6 ± 2.4% (N = 18) of initial values. Re-feeding for one day produced a definite increase in somatomedin A, with a rise in body weight. When re-fed isocalorically for 21 days with diets of different quality, a low protein diet led to smaller increases in both seum somatomedin A and body weight in comparison to those of control-, high-protein- and high fat-diets (P < 0.001). There is a positive correlation between the increase in body weight and serum somatomedin A levels (N = 70, r = 0.71, P< 0.001). The effect of growth hormone on somatomedin generation was abolished in hypophysectomized rats fed with low-protein diet. Our study suggests that protein in the diet is important for the generation of somatomedin A, which is necessary for normal growth.

scholarly journals Lasting Effects on Body Weight and Mammary Gland Gene Expression in Female Mice upon Early Life Exposure to n-3 but Not n-6 High-Fat Diets

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e55603 ◽  
Author(s):  
Mirjam Luijten ◽  
Amar V. Singh ◽  
Caleb A. Bastian ◽  
Anja Westerman ◽  
M. Michele Pisano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Mammary Gland ◽  
Early Life ◽  
High Fat ◽  
Female Mice ◽  
Early Life Exposure ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals Selective Inactivation of Socs3 in SF1 Neurons Improves Glucose Homeostasis without Affecting Body Weight

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5654-5661 ◽  
Author(s):  
Ren Zhang ◽  
Harveen Dhillon ◽  
Huali Yin ◽  
Akihiko Yoshimura ◽  
Bradford B. Lowell ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Glucose Homeostasis ◽  
Leptin Resistance ◽  
High Fat ◽  
Leptin Signaling ◽  
Leptin Sensitivity ◽  
High Fat Diets ◽  
Fat Diets

Suppressor of cytokine signaling 3 (Socs3) has been identified as a mediator of central leptin resistance, but the identity of specific neurons in which Socs3 acts to suppress leptin signaling remains elusive. The ventromedial hypothalamus (VMH) was recently shown to be an important site for leptin action because deleting leptin receptor within VMH neurons causes obesity. To examine the role of VMH Socs3 in leptin resistance and energy homeostasis, we generated mice lacking Socs3 specifically in neurons positive for steroidogenic factor 1 (SF1), which is expressed abundantly in the VMH. These mice had increased phosphorylation of signal transducer and activator of transcription-3 in VMH neurons, suggesting improved leptin signaling, and consistently, food intake and weight-reducing effects of exogenous leptin were enhanced. Furthermore, on either chow or high-fat diets, these mice had reduced food intake. Unexpectedly, energy expenditure was reduced as well. Mice lacking Socs3 in SF1 neurons, despite no change in body weight, had improved glucose homeostasis and were partially protected from hyperglycemia and hyperinsulinemia induced by high-fat diets. These results suggest that Socs3 in SF1 neurons negatively regulates leptin signaling and plays important roles in mediating leptin sensitivity, glucose homeostasis, and energy expenditure.

Free‐Choice and No‐Choice High‐Fat Diets Affect Striatal Dopamine D 2/3 Receptor Availability, Caloric Intake, and Adiposity

Obesity ◽  
2012 ◽  
Vol 20 (8) ◽  
pp. 1738-1740 ◽  
Author(s):  
Elsmarieke Giessen ◽  
Susanne E. Fleur ◽  
Kora Bruin ◽  
Wim Brink ◽  
Jan Booij
Keyword(s):  
Free Choice ◽  
Caloric Intake ◽  
Striatal Dopamine ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets
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