scholarly journals Curcumin exerts a protective effect against obesity and liver injury induced by an atherogenic diet

2021 ◽  
Vol 11 (12) ◽  
Author(s):  
María Eugenia Antona ◽  
Paula Mariela González ◽  
Cecilia Ramos ◽  
Joaquín Cabrera ◽  
Carolina Olano ◽  
...  
Keyword(s):  
Body Weight ◽  
Liver Injury ◽  
Protective Effect ◽  
Visceral Fat ◽  
Atherogenic Diet ◽  
Fat Content ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets ◽  
Visceral Fat Content

Background: Curcumin (Cur) is a natural yellow polyphenol extracted from the turmeric rhizome (Curcuma longa). Cur is known for its potential therapeutic properties as an analgesic, anti-inflammatory, antioxidant, antimicrobial, hepatoprotective, and anti-mutagenic, although some of these biological activities remain unproven. Epidemiological studies have shown a positive relationship between high-fat diets and diet-related chronic diseases. We hypothesized that some adverse effects of consuming atherogenic or high-fat diets (AD) can be ameliorated by Cur supplementation. Using an experimental model of rats, this study investigated the significance of Cur when it is given as a supplement in an AD.Methods: Healthy adult Wistar rats were randomly assigned to one of three groups. Controls (C) received a standard diet and experimental rats were fed with AD or AD+Cur for 5 weeks. Cur (100 mg/kg body weight) was given orally daily, plus piperine (5 mg/kg body weight). The effect of Cur supplementation was studied on zoometrics, visceral fat content, serum lipids profile, hepatosteatosis, liver function and oxidative status. Results: Diets did not alter energy consumption. As compared to the other groups, AD+Cur group showed a lower total visceral fat content, percentage of perirenal, mesenteric, and pelvic fat, and body weight gain (P< 0.05). Serum total cholesterol (P<0.0001), non-HDL-C (P<0.0001) levels were significantly higher in AD groups as compared with C. Serum triglycerides and HDL-C levels remained similar among groups (P>0.05). AD induced a liver injury with macrovesicular steatosis and portal inflammation. AD+Cur rats presented microvesicular steatosis with no inflammation, achieving the lowest level of alanine aminotransferase (ALT; P<0.0001) and reductions of aspartate aminotransferase (AST; P<0.0001). Liver homogenates from AD+Cur showed that Cur supplementation reduced the dichlorofluorescein diacetate (DCFH-DA) oxidation rate induced by AD by 25 % and deferoxamine and superoxide dismutase inhibited DCFH-DA. Conclusion: Cur as a dietary supplement showed a protective effect against obesity and inflammation, but its cardioprotective ability remained unproved. Cur may develop as a promising therapeutic agent for liver diseases induced by oxidative stress. This study provides supporting evidence to confirm the beneficial effects of curcumin from the point of view of functional food science.  Keywords: curcumin, liver injury, ROS, atherogenic diet, visceral fat, obesity 

Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

1994 ◽  
Vol 71 (06) ◽  
pp. 755-758 ◽  
Author(s):  
E M Bladbjerg ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen
Keyword(s):  
High Fat Diet ◽  
Fat Content ◽  
Factor Vii ◽  
Amidolytic Activity ◽  
High Fat ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Coagulant Activity ◽  
High Fat Diets ◽  
Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

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

The Protective Effect of High Fat Diets on Immature Rats Fed Thyroid

1950 ◽  
Vol 42 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Samuel M. Greenberg ◽  
Harry J. Deuel
Keyword(s):  
Protective Effect ◽  
High Fat ◽  
High Fat Diets ◽  
Immature Rats ◽  
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 Effects of Collagen Peptide Administration on Visceral Fat Content in High-Fat Diet-Induced Obese Mice

2021 ◽  
Vol 67 (1) ◽  
pp. 57-62
Author(s):  
Ran WATANABE ◽  
Mana YAMAGUCHI ◽  
Kyosuke WATANABE ◽  
Muneshige SHIMIZU ◽  
TAKAHASHI Azusa ◽  
...  
Keyword(s):  
Visceral Fat ◽  
High Fat Diet ◽  
Fat Content ◽  
Obese Mice ◽  
High Fat ◽  
Collagen Peptide ◽  
Visceral Fat Content

Elevated n-3 fatty acids in a high-fat diet attenuate the increase in PDH kinase activity but not PDH activity in human skeletal muscle

2005 ◽  
Vol 98 (1) ◽  
pp. 350-355 ◽  
Author(s):  
Erin A. Turvey ◽  
George J. F. Heigenhauser ◽  
Michelle Parolin ◽  
Sandra J. Peters
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Pyruvate Dehydrogenase ◽  
High Fat Diet ◽  
Human Skeletal Muscle ◽  
Fat Content ◽  
Pyruvate Dehydrogenase Kinase ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

We tested the hypothesis that a high-fat diet (75% fat; 5% carbohydrates; 20% protein), for which 15% of the fat content was substituted with n-3 fatty acids, would not exhibit the diet-induced increase in pyruvate dehydrogenase kinase (PDK) activity, which is normally observed in human skeletal muscle. The fat content was the same in both the regular high-fat diet (HF) and in the n-3-substituted diet (N3). PDK activity increased after both high-fat diets, but the increase was attenuated after the N3 diet (0.051 ± 0.007 and 0.218 ± 0.047 min−1 for pre- and post-HF, respectively; vs. 0.073 ± 0.016 and 0.133 ± 0.032 min−1 for pre- and post-N3, respectively). However, the active form of pyruvate dehydrogenase (PDHa) activity decreased to a similar extent in both conditions (0.93 ± 0.17 and 0.43 ± 0.09 mmol/kg wet wt pre- and post-HF; vs. 0.87 ± 0.19 and 0.39 ± 0.05 mmol/kg wet wt pre- and post-N3, respectively). This suggested that the difference in PDK activity did not affect PDHa activation in the basal state, and it was regulated by intramitochondrial effectors, primarily muscle pyruvate concentration. Muscle glycogen content was consistent throughout the study, before and after both diet conditions, whereas muscle glucose-6-phosphate, glycerol-3-phosphate, lactate, and pyruvate were decreased after the high-fat diets. Plasma triglycerides decreased after both high-fat diets but decreased to a greater extent after the N3, whereas plasma free fatty acids increased after both diets, but to a lesser extent after the N3. In summary, PDK activity is decreased after a high-fat diet that is rich in n-3 fatty acids, although PDHa activity was unaltered. In addition, our data demonstrated that the hypolipidemic effect of n-3 fatty acids occurs earlier (3 days) than previously reported and is evident even when the diet has 75% of its total energy derived from fat.

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.

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