scholarly journals Influence of habitual high dietary fat intake on endothelium-dependent vasodilation

2015 ◽  
Vol 40 (7) ◽  
pp. 711-715 ◽  
Author(s):  
Caitlin A. Dow ◽  
Brian L. Stauffer ◽  
Jared J. Greiner ◽  
Christopher A. DeSouza
Keyword(s):  
Cardiovascular Risk ◽  
Sodium Nitroprusside ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Heart Association ◽  
Underlying Mechanism ◽  
Fat Intake ◽  
High Fat ◽  
Dietary Fat Intake ◽  
Increased Risk

High-fat diets are associated with an increased risk of cardiovascular disease. A potential underlying mechanism for the increased cardiovascular risk is endothelial dysfunction. Nitric oxide (NO)-mediated endothelium-dependent vasodilation is critical in the regulation of vascular tone and overall vascular health. The aim of this study was to determine the influence of dietary fat intake on endothelium-dependent vasodilation. Forty-four middle-aged and older sedentary, healthy adults were studied: 24 consumed a lower fat diet (LFD; 29% ± 1% calories from fat) and 20 consumed a high-fat diet (HFD; 41% ± 1% calories from fat). Four-day diet records were used to assess fat intake, and classifications were based on American Heart Association guidelines (<35% of total calories from fat). Forearm blood flow (FBF) responses to acetylcholine, in the absence and presence of the endothelial NO synthase inhibitor NG-monomethyl-l-arginine (L-NMMA), as well as responses to sodium nitroprusside were determined by plethysmography. The FBF response to acetylcholine was lower (∼15%; P < 0.05) in the HFD group (4.5 ± 0.2 to 12.1 ± 0.8 mL/100 mL tissue/min) than in the LFD group (4.6 ± 0.2 to 14.4 ± 0.6 mL/100 mL tissue/min). L-NMMA significantly reduced the FBF response to acetylcholine in the LFD group (∼25%) but not in the HFD group. There were no differences between groups in the vasodilator response to sodium nitroprusside. These data indicate that a high-fat diet is associated with endothelium-dependent vasodilator dysfunction due, in part, to diminished NO bioavailability. Impaired NO-mediated endothelium-dependent vasodilation may contribute to the increased cardiovascular risk with high dietary fat intake.

scholarly journals Behavioral Feeding Circuit: Dietary Fat-Induced Effects of Inflammatory Mediators in the Hypothalamus

2020 ◽  
Vol 11 ◽  
Author(s):  
Kinning Poon
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Dietary Fatty Acids ◽  
Ingestive Behavior ◽  
Fat Intake ◽  
High Fat ◽  
Dietary Fat Intake ◽  
Orexigenic Peptide

Excessive dietary fat intake has extensive impacts on several physiological systems and can lead to metabolic and nonmetabolic disease. In animal models of ingestion, exposure to a high fat diet during pregnancy predisposes offspring to increase intake of dietary fat and causes increase in weight gain that can lead to obesity, and without intervention, these physiological and behavioral consequences can persist for several generations. The hypothalamus is a region of the brain that responds to physiological hunger and fullness and contains orexigenic neuropeptide systems that have long been associated with dietary fat intake. The past fifteen years of research show that prenatal exposure to a high fat diet increases neurogenesis of these neuropeptide systems in offspring brain and are correlated to behavioral changes that induce a pro-consummatory and obesogenic phenotype. Current research has uncovered several potential molecular mechanisms by which excessive dietary fat alters the hypothalamus and involve dietary fatty acids, the immune system, gut microbiota, and transcriptional and epigenetic changes. This review will examine the current knowledge of dietary fat-associated changes in the hypothalamus and the potential pathways involved in modifying the development of orexigenic peptide neurons that lead to changes in ingestive behavior, with a special emphasis on inflammation by chemokines.

scholarly journals Postprandial skeletal muscle metabolism following a high-fat diet in sedentary and endurance-trained males

2020 ◽  
Vol 128 (4) ◽  
pp. 872-883
Author(s):  
Mary Elizabeth Baugh ◽  
Suzanne M. Bowser ◽  
Ryan P. McMillan ◽  
Brenda M. Davy ◽  
Lauren A. Essenmacher ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Glucose Oxidation ◽  
Fat Oxidation ◽  
Fat Intake ◽  
High Fat ◽  
Substrate Metabolism ◽  
Dietary Fat Intake ◽  
Pyruvate Oxidation

Our objective was to determine the influence of a high-fat diet (HFD) on fasting and postprandial skeletal muscle substrate metabolism in endurance-trained (ET) compared with sedentary (SED) humans. SED ( n = 17) and ET ( n = 7) males were control-fed a 10-day moderate-fat diet followed by a 5-day isocaloric HFD (55% fat, 30% carbohydrate). Skeletal muscle biopsies were taken in the fasted condition and 4 h after a high-fat meal (820 kcals; 63% fat and 25% carbohydrate). Palmitate-induced suppression of pyruvate oxidation, an indication of substrate preference, and oxidation of fat and glucose were measured in homogenized skeletal muscle in fasted and fed states. Postprandial responses were calculated as percent changes from fasting to fed states. Postprandial suppression of pyruvate oxidation was maintained after the HFD in ET, but not SED skeletal muscle, suggesting greater adaptability to dietary intake changes in the former. Fasting total fat oxidation increased due to the HFD in ET skeletal muscle ( P = 0.006), which was driven by incomplete fat oxidation ( P = 0.008). Fasting fat oxidation remained unchanged in skeletal muscle of SED individuals. Yet, postprandial fat oxidation was similar between groups. Fasting glucose oxidation was elevated after the HFD in ET ( P = 0.036), but not SED, skeletal muscle. Postprandial glucose oxidation was reduced due to the HFD in SED ( P = 0.002), but not ET, skeletal muscle. These findings provide insight into differing substrate metabolism responses between SED and ET individuals and highlight the role that the prevailing diet may play in modulating fasting and postprandial metabolic responses in skeletal muscle. NEW & NOTEWORTHY The relationship between high dietary fat intake and physical activity level and their combined effect on skeletal muscle substrate metabolism remains unclear. We assessed the influence of the prevailing diet in modulating substrate oxidation in skeletal muscle of endurance-trained compared with sedentary humans during a high-fat challenge meal. Collectively, our findings demonstrate the adaptability of skeletal muscle in endurance-trained individuals to high dietary fat intake.

scholarly journals Sex differences in cardio-metabolic and cognitive parameters in rats with high-fat diet-induced metabolic dysfunction

2020 ◽  
Vol 245 (11) ◽  
pp. 977-982
Author(s):  
You Kyoung Shin ◽  
Yu Shan Hsieh ◽  
A Young Han ◽  
Soonho Kwon ◽  
Geun Hee Seol
Keyword(s):  
Blood Pressure ◽  
Sex Differences ◽  
Cognitive Impairment ◽  
Carotid Artery ◽  
Systolic Blood Pressure ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Intake ◽  
Metabolic Dysfunction ◽  
High Fat

Excessive dietary fat intake is related to metabolic dysfunction and enhances susceptibility to hypertension and cognitive impairment. Although there are sex differences in the prevalence and progression of these diseases, few studies have investigated sex differences in cardio-metabolic and cognitive parameters in rats with high-fat diet-induced metabolic dysfunction. To better reflect actual clinical conditions, sex-differences in rats with high-fat diet-induced metabolic dysfunction were evaluated. Male and female Sprague-Dawley rats were fed a high-fat diet to induce metabolic dysfunction and intraperitoneally injected with N-nitro-L-arginine methyl ester and scopolamine to model vulnerability to hypertension and cognitive impairment, respectively, whereas control rats were fed a regular diet and treated with distilled water and 0.9% saline. Male experimental rats showed significantly higher systolic blood pressure than female experimental animals. More importantly, acetylcholine-induced relaxation of carotid arteries was decreased only in the male experimental rats, revealing a significant difference compared with female experimental rats. These findings provide evidence for individualized sex-based management of patients with metabolic dysfunction and susceptibilities to hypertension and cognitive impairment. Impact statement Excessive dietary fat intake plays important roles in the process of metabolic dysfunction and increases susceptibilities to chronic diseases such as hypertension. Few previous studies, however, have accurately reflected real-world medical conditions. In addition, studies performed to date have not examined detailed sex-differences in cardio-metabolic and cognitive parameters, precluding the development of sex-tailored interventions for patients with metabolic dysfunction who are susceptible to hypertension and cognitive impairment. In this study, using rats with HFD-induced metabolic dysfunction that made them susceptible to hypertension and cognitive impairment, we demonstrate that male rats show greater impairment of acetylcholine-induced vasorelaxation of the carotid artery and systolic blood pressure compared to female rats. These findings may provide a basis for the early detection of carotid artery dysfunction and systolic blood pressure increase, especially in males.

scholarly journals Genetic Variants in Lipid Metabolism Pathways Interact with Diet to Influence Blood Lipid Concentrations in Adults with Overweight and Obesity

2020 ◽  
Vol 13 (6) ◽  
pp. 155-163
Author(s):  
Bridget A. Hannon ◽  
Caitlyn G. Edwards ◽  
Sharon V. Thompson ◽  
Sarah K. Burke ◽  
Nicholas A. Burd ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Dietary Intake ◽  
Dietary Fat ◽  
Genetic Variants ◽  
Blood Lipid ◽  
Overweight And Obesity ◽  
Cardiometabolic Health ◽  
Fat Intake ◽  
Dietary Fat Intake ◽  
Increased Risk

<b><i>Introduction:</i></b> The effect of various types of dietary fat on cardiometabolic health continues to be debated, due in part to the high heterogeneity of results following clinical trials investigating the effects of saturated (SFA) and unsaturated fat intake. This variability may be due to genetic differences. Individuals with obesity are at an increased risk for adverse cardiometabolic health and dyslipidemia, and often present with the combined phenotype of elevated triglyceride (TG) and decreased high-density lipoprotein (HDL) cholesterol concentrations. Studying genetic variants relevant to lipid and lipoprotein metabolism can elucidate the mechanisms by which diet might interact with genotype to influence these phenotypes. The objective of this study was to determine relationships of genetic variation, dietary fat intake, and blood lipid concentrations in adults with overweight and obesity. <b><i>Methods:</i></b> Genomic DNA, blood lipid concentrations (HDL and TG), and 7-day diet records were obtained from 101 adults (25–45 years of age) with overweight or obesity. Resting energy expenditure (REE) was measured using indirect calorimetry and used to determine implausible intakes using a modified Goldberg method (kilocalories/REE). Genetic variants included 23 single-nucleotide polymorphisms (SNPs) from 15 genes in lipid metabolism pathways. Variants were analyzed with dietary fat intake (total fat, SFA, monounsaturated fat [MUFA], and polyunsaturated fat [PUFA]) via regression analyses. All models were adjusted for age, sex, ancestry, visceral adipose tissue mass, and total kilocalorie intake. The Bonferroni correction was applied for multiple comparisons. <b><i>Results:</i></b> Two interactions were detected for TG concentrations. Five gene-diet interactions were associated with HDL concentrations. There was a significant interaction detected between the rs5882 variant of cholesterol-esterase transfer protein (<i>CETP</i>) and MUFA intake to associate with TG concentrations (interaction <i>p</i> = 0.004, <i>R</i><sup>2</sup> = 0.306). Among carriers of the <i>CETP-</i>rs5882 major allele (G), TG concentrations were significantly lower in individuals consuming more than the median MUFA intake (31 g/day) than in those with an intake below the median. Total dietary fat intake interacted with the rs13702 polymorphism of lipoprotein lipase (<i>LPL</i>) to associate with HDL concentrations (interaction <i>p</i> = 0.041, <i>R</i><sup>2</sup> = 0.419), by which individuals with the risk allele (G) had significantly higher HDL concentrations when consuming a higher-fat diet (&#x3e;92 g/day) than those with a lower-fat diet (56 ± 3 vs. 46 ± 2 mg/dL, <i>p</i> = 0.033). <b><i>Conclusions:</i></b> Interactions between dietary intake and genes in lipid metabolism pathways were found to be associated with blood lipid concentrations in adults with overweight and obesity. Fatty acid intake may not modulate blood lipid concentrations uniformly across all individuals. Additional research is needed to determine the biological causes of individual variability in response to dietary intake. Understanding the influence of nutrigenetic interactions on dyslipidemia can aid in the development and implementation of personalized dietary strategies to improve health.

scholarly journals The crosstalk between the gut microbiota and lipids

OCL ◽  
2020 ◽  
Vol 27 ◽  
pp. 70
Author(s):  
Philippe Gérard
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Intake ◽  
Human Intestine ◽  
Microbiota Composition ◽  
High Fat ◽  
Potential Health ◽  
Different Types ◽  
Total Fat

The human intestine harbours a complex and diverse bacterial community called the gut microbiota. This microbiota, stable during the lifetime, is specific of each individual despite the existence of a phylogenetic core shared by the majority of adults. The influence of the gut microbiota on host’s physiology has been largely studied using germfree animals and studies using these animal models have revealed that the effects of lipids on host physiology are microbiota-dependent. Studies in mice have also shown that a high-fat diet rapidly and reproducibly alters the gut microbiome. In humans, dietary fat interventions did not lead to strong and consistent modifications of the microbiota composition. Nevertheless, an association between total fat intake and the reduction of the microbiota richness has been repeatedly found. Interestingly, different types of fat exert different or even opposite effects on the microbiota. Concurrently, the gut microbiota is able to convert the lipids entering the colon, including fatty acids or cholesterol, leading to the production of metabolites with potential health effects.

scholarly journals C/EBPβ regulates hypertrophic versus hyperplastic fat tissue growth

2020 ◽  
Author(s):  
Christine Müller ◽  
Laura M. Zidek ◽  
Sabrina Eichwald ◽  
Cornelis F. Calkhoven
Keyword(s):  
Cardiovascular Diseases ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Tissue Growth ◽  
Fat Intake ◽  
Fat Tissue ◽  
High Fat ◽  
Increased Risk ◽  
Healthy Obese ◽  
Adipocyte Hyperplasia

AbstractChronic obesity is correlated with severe metabolic and cardiovascular diseases as well as with an increased risk for developing cancers. Obesity is usually characterized by fat accumulation in enlarged - hypertrophic – adipocytes that are a source of inflammatory mediators, which is seen as causal for developing metabolic disorders. Yet, in certain healthy obese individuals fat is stored in metabolically more favorable hyperplastic fat tissue that contains an increased number of smaller adipocytes that are less inflamed. In a previous study we demonstrated that C/EBPβ-LIP deficient, yet C/EBPβ-LAP proficient mice show an expanded health and lifespan. Here we show that in mice on a high-fat diet LIP-deficiency results in adipocyte hyperplasia as well as efficient fat storage in subcutaneous depots associated with metabolic and inflammatory improvements. Our data identify C/EBPβ as a regulator of adipocyte fate in response to increased fat intake, which has major implications for metabolic health and aging.

scholarly journals The role of high-fat diets and physical activity in the regulation of body weight

2000 ◽  
Vol 84 (4) ◽  
pp. 417-427 ◽  
Author(s):  
Patrick Schrauwen ◽  
Klaas R. Westerterp
Keyword(s):  
Physical Activity ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Oxidation ◽  
Fat Intake ◽  
High Fat ◽  
High Fat Diets ◽  
Prevalence Of Obesity ◽  
Fat Diets

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.

High-fat feeding alters both basal and stress-induced hypothalamic-pituitary-adrenal activity in the rat

1997 ◽  
Vol 273 (6) ◽  
pp. E1168-E1177 ◽  
Author(s):  
Beth M. Tannenbaum ◽  
David N. Brindley ◽  
Gloria S. Tannenbaum ◽  
Mary F. Dallman ◽  
M. Dawn McArthur ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Male Rats ◽  
Fat Intake ◽  
High Fat ◽  
Hypothalamic Pituitary Adrenal ◽  
Resistance To Insulin ◽  
Artery Disease ◽  
Fat Feeding

High-fat feeding induces insulin resistance and increases the risk for the development of diabetes and coronary artery disease. Glucocorticoids exacerbate this hyperinsulinemic state, rendering an individual at further risk for chronic disease. The present studies were undertaken to determine whether dietary fat-induced increases in corticosterone (B) reflect alterations in the regulatory components of the hypothalamic-pituitary-adrenal (HPA) axis. Adult male rats were maintained on a high-fat (20%) or control (4%) diet for varying periods of time. Marked elevations in light-phase spontaneous basal B levels were evident as early as 7 days after fat diet onset, and B concentrations remained significantly elevated up to 21 days after fat diet onset compared with controls. In contrast, there were no significant effects on any parameters of spontaneous growth hormone secretory profiles, thus providing support for the specificity of the effects on the HPA axis. In a second study, all groups of rats fed the high-fat diet for 1, 9, or 12 wk exhibited significantly elevated levels of plasma adrenocorticotropic hormone, B, fatty acid, and glucose before, during, and/or at 20, 60, and/or 120 min after the termination of a restraint stress. Furthermore, 12-wk fat-fed animals showed a significant resistance to insulin compared with normally fed controls. There were no differences in negative feedback efficacy in high-fat-fed rats vs. controls. Taken together, these results suggest that dietary fat intake acts as a background form of chronic stress, elevating basal B levels and enhancing HPA responses to stress.

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