A Gut Lipid Messenger Links Excess Dietary Fat to Dopamine Deficiency

Science ◽  
2013 ◽  
Vol 341 (6147) ◽  
pp. 800-802 ◽  
Author(s):  
Luis A. Tellez ◽  
Sara Medina ◽  
Wenfei Han ◽  
Jozelia G. Ferreira ◽  
Paula Licona-Limón ◽  
...  
Keyword(s):  
Dietary Fat ◽  
Dopamine Release ◽  
Oral Intake ◽  
Reward Sensitivity ◽  
Dietary Fats ◽  
Fat Intake ◽  
High Fat ◽  
Physiological Mechanisms ◽  
Reward Value ◽  
Excessive Intake

Excessive intake of dietary fats leads to diminished brain dopaminergic function. It has been proposed that dopamine deficiency exacerbates obesity by provoking compensatory overfeeding as one way to restore reward sensitivity. However, the physiological mechanisms linking prolonged high-fat intake to dopamine deficiency remain elusive. We show that administering oleoylethanolamine, a gastrointestinal lipid messenger whose synthesis is suppressed after prolonged high-fat exposure, is sufficient to restore gut-stimulated dopamine release in high-fat–fed mice. Administering oleoylethanolamine to high-fat–fed mice also eliminated motivation deficits during flavorless intragastric feeding and increased oral intake of low-fat emulsions. Our findings suggest that high-fat–induced gastrointestinal dysfunctions play a key role in dopamine deficiency and that restoring gut-generated lipid signaling may increase the reward value of less palatable, yet healthier, foods.

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 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.

Effect of diet on triolein absorption in weanling rats

1990 ◽  
Vol 258 (1) ◽  
pp. G38-G44 ◽  
Author(s):  
C. A. Flores ◽  
P. M. Brannon ◽  
M. A. Wells ◽  
M. Morrill ◽  
O. Koldovsky
Keyword(s):  
Dietary Fat ◽  
Intact Animal ◽  
Fat Intake ◽  
Fat Absorption ◽  
High Fat ◽  
High Carbohydrate ◽  
Weanling Rats ◽  
Low Carbohydrate ◽  
Triton Wr 1339

To determine the effect of altered dietary fat intake on the rate of fat absorption in the intact animal, we fed male weanling rats either a high fat-low carbohydrate (HF-LC) (calories: 67% fat, 10% carbohydrate, 20% protein) or low fat-high carbohydrate (LF-HC) (calories: 10% fat, 67% carbohydrate, 20% protein) diet for 8 days. Absorption of [14C]triolein was estimated by determining 1) 14CO2 expiration in breath, 2) intestinal triglyceride output using Triton WR-1339, an inhibitor of lipoprotein lipase, and 3) quantitating the disappearance of labeled triolein from the gastrointestinal tract. Changes in the activity of pancreatic lipase and amylase confirmed the adaptation to altered fat and carbohydrate intake. Animals fed the HF-LC diet exhibited approximately twofold greater triolein disappearance, oxidation, and intestinal triglyceride output compared with animals fed LF-HC. There was also a highly significant linear relationship between 14CO2 excretion and intestinal triglyceride output in both diet groups. These data show that high dietary fat content markedly enhances in vivo fat absorption in the weanling rat.

scholarly journals μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals

2011 ◽  
Vol 301 (1) ◽  
pp. R244-R254 ◽  
Author(s):  
Yoshihiro Katsuura ◽  
Jennifer A. Heckmann ◽  
Sharif A. Taha
Keyword(s):  
Nucleus Accumbens ◽  
Food Intake ◽  
Opioid Receptor ◽  
Third Ventricle ◽  
Fat Intake ◽  
High Fat ◽  
Drug Infusion ◽  
Physiological Mechanisms ◽  
Fatty Food ◽  
Μ Opioid Receptor

Infusion of a μ-opioid receptor (MOR) agonist into the nucleus accumbens (NAcc) drives voracious food intake, an effect hypothesized to occur through increased tastant palatability. While intake of many palatable foods is elevated by MOR stimulation, this manipulation has a preferential effect on fatty food ingestion. Consumption of high-fat foods is increased by NAcc MOR stimulation even in rats that prefer a carbohydrate-rich alternative under baseline conditions. This suggests that NAcc MOR stimulation may not simply potentiate palatability signals and raises the possibility that mechanisms mediating fat intake may be distinct from those underlying intake of other tastants. The present study was conducted to investigate the physiological mechanisms underlying the effects of NAcc MOR stimulation on fatty food intake. In experiment 1, we analyzed lick microstructure in rats ingesting Intralipid to identify the changes underlying feeding induced by infusion of a MOR-specific agonist into the NAcc. MOR stimulation in the NAcc core, but not shell, increased burst duration and first-minute licks, while simultaneously increasing the rate and duration of Intralipid ingestion. These results suggest that MOR activation in the core increases Intralipid palatability and attenuates inhibitory postingestive feedback. In experiment 2, we measured the effects of MOR stimulation in the NAcc core on consumption of nonnutritive olestra. A MOR-specific agonist dose dependently increased olestra intake, demonstrating that caloric signaling is not required for hyperphagia induced by NAcc MOR stimulation. Feeding induced by drug infusion in both experiments 1 and 2 was blocked by a MOR antagonist. In experiment 3, we determined whether MOR activation in the NAcc core could attenuate satiety-related signaling caused by infusion of the melanocortin agonist MTII into the third ventricle. Suppression of intake caused by MTII was reversed by MOR stimulation. Together, our results suggest that MOR stimulation in the NAcc core elevates fatty food intake through palatability mechanisms dependent on orosensory cues and suppression of satiety signals inhibiting food intake.

Deficits in gastrointestinal responses controlling food intake and body weight

2010 ◽  
Vol 299 (6) ◽  
pp. R1423-R1439 ◽  
Author(s):  
Mihai Covasa
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Gastrointestinal Tract ◽  
Energy Metabolism ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Dietary Fats ◽  
Hormone Release ◽  
High Fat ◽  
Chronic Ingestion

The gastrointestinal tract serves as a portal sensing incoming nutrients and relays mechanical and chemosensory signals of a meal to higher brain centers. Prolonged consumption of dietary fat causes adaptive changes within the alimentary, metabolic, and humoral systems that promote a more efficient process for energy metabolism from this rich source, leading to storage of energy in the form of adipose tissue. Furthermore, prolonged ingestion of dietary fats exerts profound effects on responses to signals involved in termination of a meal. This article reviews the effects of ingested fat on gastrointestinal motility, hormone release, and neuronal substrates. It focuses on changes in sensitivity to satiation signals resulting from chronic ingestion of high-fat diet, which may lead to disordered appetite and dysregulation of body weight.

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.

Dietary Fats Discriminate Risk for Abdominal Obesity and Glucose Metabolism among Urban Affluent Adult Males in Pune, India

2016 ◽  
Vol 53 (1) ◽  
pp. 47
Author(s):  
Prajakta Parab-Waingankar ◽  
Shobha Rao
Keyword(s):  
Glucose Metabolism ◽  
Abdominal Obesity ◽  
Fasting Blood Glucose ◽  
Dietary Fats ◽  
Abdominal Circumference ◽  
Calorie Intake ◽  
Fat Intake ◽  
Adult Males ◽  
High Fat ◽  
Cross Sectional

Indian diets have not been thoroughly investigated despite the fact that 'Nutrition Transition' parallels a rapidly escalating epidemic of obesity and Non-Communicable Diseases. Data on socio-economic background, dietary intake, BMI, Body Fat, Waist Circumference (WC), Abdominal Circumference (AC) and fasting blood estimations were recorded on 302 affluent men (30-60 years) in a cross-sectional study in Pune, India. Average daily calorie intake was lower (1714.7 ± 442 kcal) than the Recommended Dietary Allowance (ICMR, 2010) while mean fat (45.8 ± 19.1 g), carbohydrate (279.2 ± 68.3 g) and protein intakes (46.5 ± 15.1 g) were comparable. Increase in mean WC and AC (3.9 cm), in prevalence of overall obesity (49.4% to 65.4%) and in prevalence of abdominal obesity (24.7% to 40.7%) was significant (p<0.05 for all) across tertiles of total calories. But with increase in fat intake, it was only the prevalence of abdominal obesity that increased significantly (23.2% to 39.5%; p<0.05). Subjects having higher calorie intake (>1816 kcal/d) had two times higher risk for overall and abdominal adiposity while subjects having higher fat intake (>50g/d) had two times higher risk for abdominal obesity alone. Fat density but not carbohydrate, was sensitive as the prevalence of high Fasting Blood Glucose (FBG), significantly (p<0.05) increased (20.2% to 42.9%) with its increase. Additionally, the risk of high FBG was about 3 times higher (p<0.01) for high fat density (>30%). Thus, high fat density but not carbohydrate density may be an important causative factor for high rates of abdominal obesity and disturbed glucose metabolism in India.

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.

scholarly journals High-Fat Diets with Differential Fatty Acids Induce Obesity and Perturb Gut Microbiota in Honey Bee

2021 ◽  
Vol 22 (2) ◽  
pp. 834
Author(s):  
Xiaofei Wang ◽  
Zhaopeng Zhong ◽  
Xiangyin Chen ◽  
Ziyun Hong ◽  
Weimin Lin ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Honey Bee ◽  
Dietary Fat ◽  
Honey Bees ◽  
High Fat Diet ◽  
Dietary Fats ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets ◽  
Host Metabolism

HFD (high-fat diet) induces obesity and metabolic disorders, which is associated with the alteration in gut microbiota profiles. However, the underlying molecular mechanisms of the processes are poorly understood. In this study, we used the simple model organism honey bee to explore how different amounts and types of dietary fats affect the host metabolism and the gut microbiota. Excess dietary fat, especially palm oil, elicited higher weight gain, lower survival rates, hyperglycemic, and fat accumulation in honey bees. However, microbiota-free honey bees reared on high-fat diets did not significantly change their phenotypes. Different fatty acid compositions in palm and soybean oil altered the lipid profiles of the honey bee body. Remarkably, dietary fats regulated lipid metabolism and immune-related gene expression at the transcriptional level. Gene set enrichment analysis showed that biological processes, including transcription factors, insulin secretion, and Toll and Imd signaling pathways, were significantly different in the gut of bees on different dietary fats. Moreover, a high-fat diet increased the relative abundance of Gilliamella, while the level of Bartonella was significantly decreased in palm oil groups. This study establishes a novel honey bee model of studying the crosstalk between dietary fat, gut microbiota, and host metabolism.

scholarly journals Association between dietary fat and fat subtypes with the risk of breast cancer in an Iranian population: a case-control study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Maedeh Mozafarinia ◽  
Bahareh Sasanfar ◽  
Fatemeh Toorang ◽  
Amin Salehi-Abargouei ◽  
Kazem Zendehdel
Keyword(s):  
Breast Cancer ◽  
Fatty Acid ◽  
Postmenopausal Women ◽  
Dietary Fat ◽  
Case Control Study ◽  
Case Control ◽  
Dietary Fats ◽  
Fat Intake ◽  
Pufa Intake ◽  
Control Study

Abstract Aim To examine the relationship between dietary fat intake and breast cancer (BC) development. Method This case-control study included 473 women with breast cancer (pathologically confirmed) and 501 healthy subjects matched by age and residency. Dietary intakes of different types and sources of fatty acids were assessed using a validated food frequency questionnaire. The association between dietary fats and odds of BC was assessed using a logistic regression model in crude and multivariable-adjusted models. P values below 0.05 were regarded as statistically significant. Results Participants’ age and body mass index were 44.0 ± 10.8 years and 28.4 ± 5.6 kg/m2, respectively. Individuals with the highest quartile of total fat intake and polyunsaturated fatty acid (PUFA) intake were 1.50 times more at risk to develop BC than others. A positive significant association was observed between animal fat (Q4 vs. Q1, OR = 1.89, 95 % CI = 0.93–3.81), saturated fatty acid (SFA) (Q4 vs. Q1, OR = 1.70, 95 % CI = 0.88–3.30), monounsaturated fatty acid (MUFA) (Q4 vs. Q1 OR = 1.85, 95 % CI = 0.95–3.61) and PUFA intake (Q4 vs. Q1, OR = 2.12, 95 % CI = 1.05–4.27) with BC risk in postmenopausal women. However, there was no association in premenopausal women. Conclusions Total dietary fat and its subtypes might increase the risk of BC, especially in postmenopausal women. This observational study confirms the role of dietary fat in breast cancer development. Intervention studies involving different estrogen receptor subgroups are needed.

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