Weight Changes and Metabolic Outcomes in Calorie-Restricted Obese Mice Fed High-Fat Diets Containing Corn or Flaxseed Oil: Physiological Role of Sugar Replacement with Polyphenol-Rich Grape

2017 ◽  
Vol 36 (6) ◽  
pp. 422-433 ◽  
Author(s):  
Hastimansooreh Ansar ◽  
Negar Zamaninour ◽  
Abolghassem Djazayery ◽  
Hamideh Pishva ◽  
Mohammadreza Vafa ◽  
...  
Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 636
Author(s):  
Germán Domínguez-Vías ◽  
Ana Belén Segarra ◽  
Manuel Ramírez-Sánchez ◽  
Isabel Prieto

High-fat diets (HFD) have been widely associated with an increased risk of metabolic disorders and overweight. However, a high intake of sources that are rich in monounsaturated fatty acids has been suggested as a dietary agent that is able to positively influence energy metabolism and vascular function. The main objective of this study was to analyze the role of dietary fats on hepatic peptidases activities and metabolic disorders. Three diets: standard (S), HFD supplemented with virgin olive oil (VOO), and HFD supplemented with butter plus cholesterol (Bch), were administered over six months to male Wistar rats. Plasma and liver samples were collected for clinical biochemistry and aminopeptidase activities (AP) analysis. The expression of inducible nitric oxide synthase (iNOS) was also determined by Western blot in liver samples. The diet supplement with VOO did not induce obesity, in contrast to the Bch group. Though the VOO diet increased the time that was needed to return to the basal levels of plasma glucose, the fasting insulin/glucose ratio and HOMA2-%B index (a homeostasis model index of insulin secretion and valuation of β-cell usefulness (% β-cell secretion)) were improved. An increase of hepatic membrane-bound dipeptidyl-peptidase 4 (DPP4) activity was found only in VOO rats, even if no differences in fasting plasma glucagon-like peptide 1 (GLP-1) were obtained. Both HFDs induced changes in hepatic pyroglutamyl-AP in the soluble fraction, but only the Bch diet increased the soluble tyrosyl-AP. Angiotensinase activities that are implicated in the metabolism of angiotensin II (AngII) to AngIV increased in the VOO diet, which was in agreement with the higher activity of insulin-regulated-AP (IRAP) in this group. Otherwise, the diet that was enriched with butter increased soluble gamma-glutamyl transferase (GGT) and Leucyl-AP, iNOS expression in the liver, and plasma NO. In summary, VOO increased the hepatic activity of AP that were related to glucose metabolism (DPP4, angiotensinases, and IRAP). However, the Bch diet increased activities that are implicated in the control of food intake (Tyrosine-AP), the index of hepatic damage (Leucine-AP and GGT), and the expression of hepatic iNOS and plasma NO. Taken together, these results support that the source of fat in the diet affects several peptidases activities in the liver, which could be related to alterations in feeding behavior and glucose metabolism.


2014 ◽  
Vol 16 (3) ◽  
pp. 307-320 ◽  

Obesity is now epidemic worldwide. Beyond associated diseases such as diabetes, obesity is linked to neuropsychiatric disorders such as depression. Alarmingly maternal obesity and high-fat diet consumption during gestation/lactation may "program" offspring longterm for increased obesity themselves, along with increased vulnerability to mood disorders. We review the evidence that programming of brain and behavior by perinatal diet is propagated by inflammatory mechanisms, as obesity and high-fat diets are independently associated with exaggerated systemic levels of inflammatory mediators. Due to the recognized dual role of these immune molecules (eg, interleukin [IL]-6, 11-1β) in placental function and brain development, any disruption of their delicate balance with growth factors or neurotransmitters (eg, serotonin) by inflammation early in life can permanently alter the trajectory of fetal brain development. Finally, epigenetic regulation of inflammatory pathways is a likely candidate for persistent changes in metabolic and brain function as a consequence of the perinatal environment.


1961 ◽  
Vol 201 (1) ◽  
pp. 23-26 ◽  
Author(s):  
Serene Lochaya ◽  
Nicole Leboeuf ◽  
Jean Mayer ◽  
Bernard Leboeuf

Adipose tissue metabolism in vitro was studied, after substitution for several weeks of synthetic low-carbohydrate, high-fat (saturated or unsaturated) diets for the standard chow diet, in obese hyperglycemic mice and in their nonobese littermates. In tissue from nonobese mice fed the high-fat diets, glucose metabolism to CO2 and to fatty acids was diminished in the absence of added hormone, while glucose carbon incorporation to glyceride-glycerol was increased. Under insulin (0.1 unit/ml) stimulation, total glucose uptake was relatively decreased by the diets, as was glucose metabolism to CO2, to fatty acids, and to glycogen; however, glucose carbon incorporation to glyceride-glycerol was unaltered. Under epinephrine stimulation, the sum of glucose carbon recovery was less after high-fat feeding. No effect of high-fat feeding was detected on base-line rates of free fatty acid release nor on the effects of insulin or epinephrine on this process. No differences were found between the effects of saturated- or unsaturated-fat diets on any parameters. The metabolism of adipose tissue from obese mice was slightly, if at all, affected by high-fat feeding. These results are discussed in reference to the normal adaptation to low-carbohydrate, high-fat diets and to the metabolic abnormalities present in obese hyperglycemic mice.


2000 ◽  
Vol 84 (4) ◽  
pp. 417-427 ◽  
Author(s):  
Patrick Schrauwen ◽  
Klaas R. Westerterp

The prevalence of obesity is increasing in westernized societies. In the USA the age-adjusted prevalence of BMI ≫30 kg/m2 increased between 1960 and 1994 from 13 % to 23 % for people over 20 years of age. This increase in the prevalence of obesity has been attributed to an increased fat intake and a decreased physical activity. However, the role of the impact of the level of dietary fat intake on human obesity has been challenged. High-fat diets, due to their high energy density, stimulate voluntary energy intake. An increased fat intake does not stimulate its own oxidation but the fat is stored in the human body. When diet composition is isoenergetically switched from low to high fat, fat oxidation only slowly increases, resulting in positive fat balances on the short term. Together with a diminished fat oxidation capacity in pre-obese subjects, high-fat diets can therefore be considered to be fattening. Another environmental factor which could explain the increasing prevalence of obesity is a decrease in physical activity. The percentage of body fat is negatively associated with physical activity and exercise has pronounced effects on energy expenditure and substrate oxidation. High-intensity exercise, due to a lowering of glycogen stores, can lead to a rapid increase in fat oxidation, which could compensate for the consumption of high-fat diets in westernized societies. Although the consumption of high-fat diets and low physical activity will easily lead to the development of obesity, there is still considerable inter-individual variability in body composition in individuals on similar diets. This can be attributed to the genetic background, and some candidate genes have been discovered recently. Both leptin and uncoupling protein have been suggested to play a role in the prevention of diet-induced obesity. Indeed, leptin levels are increased on a high-fat diet but this effect can be attributed to the increased fat mass observed on the high-fat diet. No effect of a high-fat diet per se on leptin levels is observed. Uncoupling proteins are increased by high-fat diets in rats but no data are available in human subjects yet. In conclusion, the increased intake of dietary fat and a decreasing physical activity level are the most important environmental factors explaining the increased prevalence of obesity in westernized societies.


2014 ◽  
Vol 17 (12) ◽  
pp. 1322-1331 ◽  
Author(s):  
Yonghae Son ◽  
Min Kyung Jang ◽  
Myeong Ho Jung

2021 ◽  
Author(s):  
Yinan Hua ◽  
Jingyi Shen ◽  
Rong Fan ◽  
Rong Xiao ◽  
Weiwei Ma

Abstract Background: Excessive consumption of high-fat diets is associated with disordered metabolic responses, which may lead to chronic diseases. High-fat diets containing different types of fatty acids lead to distinct alterations in metabolic responses of gut-brain axis. Methods: In our study, normal male C57BL/6J mice were fed to multiple high fatty acid diets (long-chain and medium-chain saturated fatty acid, LCSFA and MCSFA group; n-3 and n-6 polyunsaturated fatty acid, n-3 and n-6 PUFA group; monounsaturated fatty acid, MUFA group; trans fatty acid, TFA group) and a basic diet (control, CON group) for 19 weeks. To investigate the effects of high-fat diets on metabolic responses of gut-brain axis in obese mice, blood lipids were detected by fast gas chromatography, and related proteins in brain and intestine were detected using Western blotting, ELISA, and immunochemistry analysis. Results: All high-fat diets regardless of their fatty acid composition induced obesity, lipid disorders, intestinal barrier dysfunction, and changes in gut-brain axis related factors except basal diet in mice. For example, the protein expression of zonula occludens-1 (ZO-1) in ileum in the n-3 PUFA group was higher than those in the MCSFA and CON group (all Ps < 0.05). The expressions of insulin in hippocampus and leptin in ileum in the MCSFA group were all higher than those in other groups (all Ps < 0.05). Conclusions: The high MCSFA diet had the most effect on metabolic disorders, and the high n-3 PUFA diet had the least effect on changes in metabolism.


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