Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides

2007 ◽  
Vol 292 (2) ◽  
pp. E561-E570 ◽  
Author(s):  
G.-Q. Chang ◽  
O. Karatayev ◽  
R. Ahsan ◽  
V. Gaysinskaya ◽  
Z. Marwil ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Dietary Fat ◽  
Opioid Peptides ◽  
High Fat Diet ◽  
Caloric Intake ◽  
High Fat ◽  
Caloric Density ◽  
Low Fat Diet ◽  
Diet Intake

The opioid peptides enkephalin (ENK) and dynorphin (DYN), when injected into the hypothalamus, are known to stimulate feeding behavior and preferentially increase the ingestion of a high-fat diet. Studies of another peptide, galanin (GAL), with similar effects on feeding demonstrate that a high-fat diet, in turn, can stimulate the expression of this peptide in the hypothalamus. The present study tested different diets and variable periods of high- vs. low-fat diet consumption to determine whether the opioid peptides respond in a similar manner as GAL. In six experiments, the effects of dietary fat on ENK and DYN were examined in three hypothalamic areas: the paraventricular nucleus (PVN), perifornical hypothalamus (PFH), and arcuate nucleus (ARC). The results demonstrated that the ingestion of a high-fat diet increases gene expression and peptide levels of both ENK and DYN in the hypothalamus. The strongest and most consistent effect is seen in the PVN. In this nucleus, ENK and DYN are increased by 50–100% after 1 wk, 1 day, 60 min, and even 15 min of high-fat diet consumption. While showing some effect in the PFH, these peptides in the ARC are considerably less responsive, exhibiting no change in response to the briefer periods of diet intake. This effect of dietary fat on PVN opioids can be observed with diets equal in caloric density and palatability and without a change in caloric intake, body weight, fat pad weight, or levels of insulin or leptin. The data reveal a strong and consistent association between these peptides and a rise in circulating levels of triglycerides, supporting a role for these lipids in the fat-induced stimulation of opioid peptides in the PVN, similar to GAL.

scholarly journals The role of dietary fat in obesity-induced insulin resistance

2016 ◽  
Vol 311 (6) ◽  
pp. E989-E997 ◽  
Author(s):  
Denise E. Lackey ◽  
Raul G. Lazaro ◽  
Pingping Li ◽  
Andrew Johnson ◽  
Angelina Hernandez-Carretero ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Caloric Intake ◽  
High Fat ◽  
Low Fat ◽  
Feeding Method ◽  
Low Fat Diet ◽  
Obesity And Diabetes

Consumption of excess calories results in obesity and insulin resistance and has been intensively studied in mice and humans. The objective of this study was to determine the specific contribution of dietary fat rather than total caloric intake to the development of obesity-associated insulin resistance. We used an intragastric feeding method to overfeed excess calories from a low-fat diet (and an isocalorically matched high-fat diet) through a surgically implanted gastric feeding tube to generate obesity in wild-type mice followed by hyperinsulinemic-euglycemic clamp studies to assess the development of insulin resistance. We show that overfeeding a low-fat diet results in levels of obesity similar to high-fat diet feeding in mice. However, despite a similar body weight, obese high-fat diet-fed mice are more insulin resistant than mice fed an isocaloric low-fat diet. Therefore, increased proportion of calories from dietary fat further potentiates insulin resistance in the obese state. Furthermore, crossover diet studies revealed that reduction in dietary fat composition improves glucose tolerance in obesity. In the context of the current obesity and diabetes epidemic, it is particularly important to fully understand the role of dietary macronutrients in the potentiation and amelioration of disease.

scholarly journals Effects of dietary fat quantity and composition on fasting and postprandial levels of coagulation factor VII and serum choline-containing phospholipids

2003 ◽  
Vol 90 (2) ◽  
pp. 329-336 ◽  
Author(s):  
Anja Schou Lindman ◽  
Hanne Müller ◽  
Ingebjørg Seljeflot ◽  
Hans Prydz ◽  
Marit Veierød ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Coagulation Factor ◽  
Factor Vii ◽  
High Fat ◽  
Coagulation Factor Vii ◽  
Low Fat Diet

Dietary fat influences plasma levels of coagulation factor VII (FVII) and serum phospholipids (PL). It is, however, unknown if the fat-mediated changes in FVII are linked to PL. The present study aimed to investigate the effects of dietary fat on fasting and postprandial levels of activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII protein (FVIIag) and choline-containing PL (PC). In a randomized single-blinded crossover-designed study a high-fat diet (HSAFA), a low-fat diet (LSAFA), both rich in saturated fatty acids, and a high-fat diet rich in unsaturated fatty acids (HUFA) were consumed for 3 weeks. Twenty-five healthy females, in which postprandial responses were studied in a subset of twelve, were included. The HSAFA diet resulted in higher levels of fasting FVIIa and PC compared with the LSAFA and the HUFA diets (all comparisonsP≤0·01). The fasting PC levels after the LSAFA diet were also higher than after the HUFA diet (P<0·001). Postprandial levels of FVIIa and PC were highest on the HSAFA diet and different from LSAFA and HUFA (all comparisonsP≤0·05). Postprandial FVIIa was higher on the HUFA compared with the LSAFA diet (P<0·03), whereas the HUFA diet resulted in lower postprandial levels of PC than the LSAFA diet (P<0·001). Significant correlations between fasting levels of PC and FVIIc were found on all diets, whereas FVIIag was correlated to PC on the HSAFA and HUFA diet. The present results indicate that dietary fat, both quality and quantity, influences fasting and postprandial levels of FVIIa and PC. Although significant associations between fasting FVII and PC levels were found, our results do not support the assumption that postprandial FVII activation is linked to serum PC.

Acute changes in the response to peripheral leptin with alteration in the diet composition

2001 ◽  
Vol 280 (2) ◽  
pp. R504-R509 ◽  
Author(s):  
L. Lin ◽  
R. Martin ◽  
A. O. Schaffhauser ◽  
D. A. York
Keyword(s):  
Food Intake ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Corticosterone Level ◽  
Inhibitory Response ◽  
Leptin Resistance ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Alternative Diet

Dietary induced obesity in rodents is associated with a resistance to leptin. We have investigated the hypothesis that dietary fat per se alters the feeding response to peripheral leptin in rats that were fed either their habitual high- or low-fat diet or were naively exposed to the alternative diet. Osborne-Mendel rats were adapted to either high- or low-fat diet. Food-deprived rats were given either leptin (0.5 mg/kg body wt ip) or saline, after which they were provided with either their familiar diet or the alternative diet. Food intake of rats adapted and tested with the low-fat diet was reduced 4 h after leptin injection, whereas rats adapted and tested with a high-fat diet did not respond to leptin. Leptin was injected again 1 and 5 days after the high-fat diet-adapted rats were switched to the low-fat diet. Leptin reduced the food intake on both days. In contrast, when low-fat diet-adapted rats were switched to a high-fat diet, the leptin inhibitory response was present on day 1 but not observed on day 5. Peripheral injection of leptin increased serum corticosterone level and decreased hypothalamic neuropeptide Y mRNA expression in rats fed the low-fat but not the high-fat diet for 20 days. The data suggest that dietary fat itself, rather than obesity, may induce leptin resistance within a short time of exposure to a high-fat diet.

scholarly journals Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

2016 ◽  
Vol 310 (11) ◽  
pp. E886-E899 ◽  
Author(s):  
Pia Kiilerich ◽  
Lene Secher Myrmel ◽  
Even Fjære ◽  
Qin Hao ◽  
Floor Hugenholtz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Low Protein

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.

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 Germ-Free Swiss Webster Mice on a High-Fat Diet Develop Obesity, Hyperglycemia, and Dyslipidemia

2020 ◽  
Vol 8 (4) ◽  
pp. 520
Author(s):  
Isabelle E. Logan ◽  
Gerd Bobe ◽  
Cristobal L. Miranda ◽  
Stephany Vasquez-Perez ◽  
Jaewoo Choi ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Glucose Absorption ◽  
Feed Conversion ◽  
High Fat ◽  
Germ Free ◽  
Low Fat Diet ◽  
Established Risk Factor ◽  
Diet Induced Obesity ◽  
Hepatic Triacylglycerol

A calorie-dense diet is a well-established risk factor for obesity and metabolic syndrome (MetS), whereas the role of the intestinal microbiota (IMB) in the development of diet-induced obesity (DIO) is not completely understood. To test the hypothesis that Swiss Webster (Tac:SW) mice can develop characteristics of DIO and MetS in the absence of the IMB, we fed conventional (CV) and germ-free (GF) male Tac:SW mice either a low-fat diet (LFD; 10% fat derived calories) or a high-fat diet (HFD; 60% fat derived calories) for 10 weeks. The HFD increased feed conversion and body weight in GF mice independent of the increase associated with the microbiota in CV mice. In contrast to CV mice, GF mice did not decrease feed intake on the HFD and possessed heavier fat pads. The HFD caused hyperglycemia, hyperinsulinemia, and impaired glucose absorption in GF mice independent of the increase associated with the microbiota in CV mice. A HFD also elevated plasma LDL-cholesterol and increased hepatic triacylglycerol, free fatty acids, and ceramides in all mice, whereas hypertriglyceridemia and increased hepatic medium and long-chain acylcarnitines were only observed in CV mice. Therefore, GF male Tac:SW mice developed several detrimental effects of obesity and MetS from a high-fat, calorie dense diet.

scholarly journals Transection of Gustatory Nerves Differentially Affects Dietary Fat Intake in Obesity-Prone and Obesity-Resistant Rats

2020 ◽  
Vol 45 (7) ◽  
pp. 541-548
Author(s):  
Allyson Schreiber ◽  
Hugh Douglas Braymer ◽  
Stefany D Primeaux
Keyword(s):  
Dietary Fat ◽  
Caloric Intake ◽  
Afferent Input ◽  
Fat Intake ◽  
Fungiform Papillae ◽  
Dietary Fat Intake ◽  
Low Fat Diet ◽  
Current Prevalence ◽  
Prevalence Of Obesity

Abstract The current prevalence of obesity has been linked to the consumption of highly palatable foods and may be mediated by a dysregulated or hyposensitive orosensory perception of dietary fat, thereby contributing to the susceptibility to develop obesity. The goal of the current study was to investigate the role of lingual taste input in obesity-prone (OP, Osborne-Mendel) and obesity-resistant (OR, S5B/Pl) rats on the consumption of a high-fat diet (HFD). Density of fungiform papillae was assessed as a marker of general orosensory input. To determine if orosensory afferent input mediates dietary fat intake, surgical transection of the chorda tympani and glossopharyngeal nerves (GLX/CTX) was performed in OP and OR rats and HFD caloric intake and body weight were measured. Fungiform papillae density was lower in OP rats, compared with OR rats. GLX/CTX decreased orosensory input in both OP and OR rats, as measured by an increase in the intake of a bitter, quinine solution. Consumption of low-fat diet was not altered by GLX/CTX in OP and OR rats; however, GLX/CTX decreased HFD intake in OR, without altering HFD intake in OP rats. Overall, these data suggest that inhibition of orosensory input in OP rats do not decrease fat intake, thereby supporting that idea that hyposensitive and/or dysregulated orosensory perception of highly palatable foods contribute to the susceptibility to develop obesity.

Chemical lesion of visceral afferents causes transient overconsumption of unfamiliar high-fat diets in rats

1997 ◽  
Vol 272 (5) ◽  
pp. R1657-R1663 ◽  
Author(s):  
M. Chavez ◽  
L. Kelly ◽  
D. A. York ◽  
H. R. Berthoud
Keyword(s):  
Negative Feedback ◽  
High Fat Diet ◽  
Visceral Afferents ◽  
Control Mechanisms ◽  
Sprague Dawley ◽  
High Fat ◽  
Chemical Lesion ◽  
Diet Intake ◽  
Fat Diets

Because it is commonly assumed that the major role of visceral afferents in food intake control is to terminate meals by carrying negative-feedback signals to the brain, we hypothesized that overconsumption should occur in rats with chemically lesioned visceral afferents if they were presented with an unfamiliar diet. Adult male Sprague-Dawley (SD) rats were treated with multiple doses of capsaicin or vehicle as a control. Five weeks later, a series of 3-h feeding tests after 24-h deprivation was carried out, first with chow and then with either a solid (vegetable shortening) or liquid (Ensure) unfamiliar high-fat diet. Both groups consumed similar amounts of their powdered chow maintenance diet, but capsaicin-treated rats consumed at least 50% more of either high-fat diet than vehicle controls (P < 0.01) at the beginning of the first trial. During second and third trials with the now-familiar high-fat diet, intake was no longer significantly different between the two groups, suggesting rapid engagement of redundant control mechanisms. These results support a role of capsaicin-sensitive visceral afferents in providing negative feedback for early meal termination during the ingestion of unfamiliar diets.

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