Abstract 155: Cardiac Function And Calcium Handling in Obesity-Resistant rats

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Andre Leopoldo ◽  
Felipe de Sá ◽  
Wagner Estevam ◽  
Bruno Jacobsen ◽  
Artur Ferron ◽  
...  

Experimental studies have demonstrated that obesity induced by different types of high-fat and/or high-energy diets also lead to myocardial dysfunction. Nevertheless, few studies have evaluated the myocardial function in obesity-resistant rats. Moreover, the mechanisms underlying the participation of calcium (Ca 2+ ) handling on cardiac function in this model remain unknown. The aim of this study was to investigate in rodent model of obesity-resistant. In addition, as obesity-resistant group is fed a high-fat diet but did not become obese, this study tested whether obesity-resistant model develops cardiac abnormalities and impairment of calcium handling as obesity-prone. Male 30-day-old Wistar rats were fed standard (C) and alternately four palatable unsaturated high-fat diets (Ob) for 15 weeks. After experimental protocol, Ob rats consuming the unsaturated high-fat diets were ranked based on adiposity index. Rats on the unsaturated high-fat diets exhibiting the greatest adiposity index were referred to as OP, whereas those exhibiting the lowest adiposity index were referred to as OR. Obesity was determined by adiposity index and comorbidities were evaluated. Myocardial function was evaluated in isolated left ventricle papillary muscles under basal conditions and after inotropic and lusitropic maneuvers. After 15 weeks, final body weight, total body fat, adiposity index, triglycerides levels and heart weight were significantly greater in OP rats than C and OR rats, however, there was no change in systolic blood pressure between groups. The C, OP and OR muscles developed similar baseline data, but myocardial responsiveness to post-rest contraction stimulus was compromised in OP rats. In conclusion, obesity-resistant model by unsaturated high-fat diet, after 15 weeks, does not display nutritional and metabolic characteristics of obesity-prone. Furthermore, obesity-resistant does not promote cardiac abnormalities and impairment of calcium handling visualized in obesity-prone.

1994 ◽  
Vol 71 (06) ◽  
pp. 755-758 ◽  
Author(s):  
E M Bladbjerg ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen

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.


2021 ◽  
Author(s):  
Qiao Jie ◽  
Yue-Zhong Ren ◽  
Yi-wen Wu

High-fat diets(HFD)are defined as lipids accounting for exceeded 30% of total energy in-take, and current research is mostly 45% and 60%. With a view of the tendency that patients who...


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Murali ◽  
Carla Taylor ◽  
Peter Zahradka ◽  
Jeffrey Wigle

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Sarah Wong ◽  
Rafael de Cabo ◽  
Michel Bernier ◽  
Alberto Diaz-Ruiz ◽  
Tyler Rhinesmith ◽  
...  

Abstract Objectives 4:10 periodic fasting schedule is proposed to improve biomarkers of healthspan through metabolic flexibility in mice on both standard and high fat diets. Methods Our study adopted the 4:10 fasting schedule using the fasting-mimicking diet (FMD) as our model. FMD is a plant-based, low-protein, and low-sugar diet regime implemented for four days every two-week cycle. Its regenerative effect is observed in the refeeding phase following starvation, allowing for the breakdown of cells via increased autophagy. In comparison to stricter fasting regimes such as intermittent fasting, chronic caloric restriction, and periodic fasting, FMD is well-tolerated in the clinical setting. 74 12-month old C57BL/6 mice were randomized into two diet groups: standard diet or high-fat diet. For 4 days out of every fourteen days, the mice were severely caloric restricted and refed with ad-libitum of either standard or high fat diets for the remaining 10 days, matching the controls who were fixed on the ad-libitum diet. The 4:10 fasting schedule was repeated 11 times before the mice were sacrificed. To measure metabolic flexibility, metabolic cages, ELISA, and glucose meters were used. Results Body weight and composition, metabolic flexibility, and insulin sensitivity indicate differences between fasting on diet composition. Not only did those on the fasting high-fat diet (FHFD) remain overweight, identical to their HFD controls, insulin sensitivity was also attenuated in FHFD groups. Fasting standard diet (FSD) had a reduction of 5% in body weight and 15% in body fat. Carbohydrate and lipid metabolism differences indicated by the respiratory exchange ratio as well as motor function performance differences further support the positive impact of fasting on SD groups, not HFD groups. Characteristic of positive healthspan biomarkers, reduced leptin and improved insulin sensitivity was observed with FSD, not FHFD. Conclusions We found that while the FMD schedule improved healthspan as indicated by biomarkers of healthy aging for mice on the standard diet, it could not counteract the negative health effects of the obesogenic diet. These results demonstrate the importance of not only time of feeding but also diet composition in respect to healthspan. Funding Sources National Institute on Aging (NIA) – National Institutes of Health (NIH).


2017 ◽  
Vol 6 ◽  
Author(s):  
Thao Duy Nguyen ◽  
Olena Prykhodko ◽  
Frida Fåk Hållenius ◽  
Margareta Nyman

AbstractButyric acid has been shown to have suppressive effects on inflammation and diseases related to the intestinal tract. The aim of the present study was to investigate whether supplementation of two glycerol esters, monobutyrin (MB) and tributyrin (TB), would reach the hindgut of rats, thus having an effect on the caecal profile of SCFA, microbiota composition and some risk markers associated with chronic inflammation. For this purpose, rats were fed high-fat diets after adding MB (1 and 5 g/kg) and TB (5 g/kg) to a diet without any supplementation (high-fat control; HFC). A low-fat (LF) diet was also included. In the liver, total cholesterol concentrations, LDL-cholesterol concentrations, LDL:HDL ratio, and succinic acid concentrations were reduced in rats given the MB and TB (5 g/kg) diets, compared with the group fed the HFC diet. These effects were more pronounced in MB than TB groups as also expressed by down-regulation of the gene Cyp8b1. The composition of the caecal microbiota in rats fed MB and TB was separated from the group fed the HFC diet, and also the LF diet, as evidenced by the absence of the phylum TM7 and reduced abundance of the genera Dorea (similar to LF-fed rats) and rc4-4. Notably, the caecal abundance of Mucispirillum was markedly increased in the MB group compared with the HFC group. The results suggest that dietary supplementation of MB and TB can be used to counteract disturbances associated with a HFC diet, by altering the gut microbiota, and decreasing liver lipids and succinic acid concentrations.


2014 ◽  
Vol 5 (3) ◽  
pp. 229-239 ◽  
Author(s):  
K. M. Platt ◽  
R. J. Charnigo ◽  
K. J. Pearson

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.


1992 ◽  
Vol 263 (4) ◽  
pp. R785-R789 ◽  
Author(s):  
T. A. Buchanan ◽  
J. S. Fisler ◽  
S. Underberger ◽  
G. F. Sipos ◽  
G. A. Bray

To determine whether whole body insulin sensitivity differs between a rat strain that does not (S 5B/Pl) and a strain that does [Osborne-Mendel (OM)] become obese when eating a high-fat diet, we performed euglycemic clamp studies in animals from each strain during low- and high-fat feeding. Clamps were performed after 2 days ("initial clamp") and 9 days ("final clamp") on each diet. Plasma glucose and insulin levels during the final 60 min of initial and final clamps were similar in S 5B/Pl and OM rats regardless of diet. Insulin sensitivity, measured as the glucose clearance rate during the final 60 min of the clamp, averaged 35 +/- 3 ml.kg-1.min-1 in S 5B/Pl rats after 2 days on a low-fat diet. This did not change significantly during an additional 7 days on the low-fat diet. The high-fat diet was associated with a 13% reduction in insulin sensitivity after 2 days and a 30% reduction after 9 days in S 5B/Pl rats. OM rats exhibited similar patterns of insulin sensitivity during low- and high-fat diets, albeit at lower insulin sensitivity overall (P < 0.0005 vs. S 5B/Pl). Mean glucose clearance after 2 days on the low-fat diet was 27 +/- 2 mg.kg-1.min-1 and did not change significantly during seven more days of low-fat feeding. The high-fat diet was associated with a 19% reduction in glucose clearance after 2 days and a 38% reduction after 9 days in OM rats. The magnitude of reduction in insulin sensitivity during high-fat diets did not differ significantly between strains.(ABSTRACT TRUNCATED AT 250 WORDS)


2019 ◽  
Vol 60 (6) ◽  
pp. 1112-1120 ◽  
Author(s):  
Chandramohan Chitraju ◽  
Tobias C. Walther ◽  
Robert V. Farese

Mammals store metabolic energy as triacylglycerols (TGs) in adipose tissue. TG synthesis is catalyzed by the evolutionarily unrelated acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes DGAT1 and DGAT2, which catalyze the same reaction and account for nearly all TG synthesis. The reasons for their convergent evolution to synthesize TGs remain unclear. Mice lacking DGAT1 are viable with reduced fat stores of TGs, whereas DGAT2 KO mice die postnatally just after birth with >90% reduction of TGs, suggesting that DGAT2 is the predominant enzyme for TG storage. To better understand the functional differences between the DGATs, we studied mice fed chow or high-fat diets lacking either enzyme in adipose tissue. Unexpectedly, mice lacking DGAT2 in adipocytes have normal TG storage and glucose metabolism on regular or high-fat diets, indicating DGAT2 is not essential for fat storage. In contrast, mice lacking DGAT1 in adipocytes have normal TG storage on a chow diet but moderately decreased body fat accompanied by glucose intolerance when challenged with a high-fat diet. The latter changes were associated with the activation of ER stress pathways. We conclude that DGAT1 and DGAT2 can largely compensate for each other for TG storage but that DGAT1 uniquely has an important role in protecting the ER from the lipotoxic effects of high-fat diets.


1942 ◽  
Vol 75 (2) ◽  
pp. 179-189 ◽  
Author(s):  
David P. Earle ◽  
Joseph Victor

1. The effect of 9 different diets on the liver lesions resulting from excess dietary cystine has been studied in 130 rats. 2. The incidence and severity of each of the following liver lesions were varied by changes in the composition of diets containing 5 or 10 per cent cystine: (a) Hemorrhage was least severe with low fat diets. (b) Necrosis was most severe with synthetic diets. (c) Cirrhosis was delayed by a diet high in lard, 20 per cent, and cod liver oil, 5 per cent, but not by a diet high in butter, 25 per cent. (d) Fatty infiltration was found consistently only with low protein, high fat diets. In other words, the pathogenesis of the liver lesion due to excess dietary cystine can be modified by diet. 3. In the presence of cystine as 5 per cent of a low protein, high fat diet, 1 per cent choline inhibited fatty infiltration but did not protect the liver against damage by cystine. 4. In these experiments there was no apparent correlation between fatty infiltration of the liver and the incidence or degree of cirrhosis.


2005 ◽  
Vol 98 (1) ◽  
pp. 350-355 ◽  
Author(s):  
Erin A. Turvey ◽  
George J. F. Heigenhauser ◽  
Michelle Parolin ◽  
Sandra J. Peters

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.


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