Decreased responsiveness to dietary fat in Otsuka Long-Evans Tokushima fatty rats lacking CCK-A receptors

1999 ◽  
Vol 277 (4) ◽  
pp. R1144-R1151 ◽  
Author(s):  
Gary J. Schwartz ◽  
Andrew Whitney ◽  
Chris Skoglund ◽  
Thomas W. Castonguay ◽  
Timothy H. Moran
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Corn Oil ◽  
High Fat ◽  
Oletf Rats ◽  
Glucose Intake ◽  
Long Evans ◽  
Fat Feeding ◽  
Cck Release ◽  
Subsequent Intake

Adult Otsuka Long-Evans Tokushima fatty (OLETF) rats lack functional cholecystokinin A (CCK-A) receptors, are diabetic, hyperphagic, and obese, and have patterns of ingestion consistent with a satiety deficit secondary to CCK insensitivity. Because dietary fat potently stimulates CCK release, we examined how dietary fat modulates feeding in adult male OLETF rats and their lean [Long-Evans Tokushima (LETO)] controls. High-fat feeding produced sustained overconsumption of high-fat diet (30% corn oil in powdered chow) over a 3-wk period in OLETF but not LETO rats. We then assessed the ability of gastric gavage (5 ml, 1–2 kcal/ml × 15 s) or duodenal preloads (1 kcal/ml, 0.44 ml/min × 10 min) of liquid carbohydrate (glucose), protein (peptone), or fat (Intralipid) to suppress subsequent 30-min 12.5% glucose intake in both strains. In OLETF rats, gastric and duodenal fat preloads were significantly less effective in suppressing subsequent intake than were equicaloric peptone or glucose. These results demonstrate that OLETF rats fail to compensate for fat calories and suggest that their hyperphagia and obesity may stem from a reduced ability to process nutrient-elicited gastrointestinal satiety signals.

High-fat diet-induced muscle insulin resistance: relationship to visceral fat mass

2000 ◽  
Vol 279 (6) ◽  
pp. R2057-R2065 ◽  
Author(s):  
Jong-Yeon Kim ◽  
Lorraine A. Nolte ◽  
Polly A. Hansen ◽  
Dong-Ho Han ◽  
Kevin Ferguson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fish Oil ◽  
Fat Mass ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Corn Oil ◽  
High Fat ◽  
Muscle Insulin Resistance ◽  
Visceral Fat Accumulation ◽  
Fat Feeding

It has been variously hypothesized that the insulin resistance induced in rodents by a high-fat diet is due to increased visceral fat accumulation, to an increase in muscle triglyceride (TG) content, or to an effect of diet composition. In this study we used a number of interventions: fish oil, leptin, caloric restriction, and shorter duration of fat feeding, to try to disassociate an increase in visceral fat from muscle insulin resistance. Substituting fish oil (18% of calories) for corn oil in the high-fat diet partially protected against both the increase in visceral fat and muscle insulin resistance without affecting muscle TG content. Injections of leptin during the last 4 days of a 4-wk period on the high-fat diet partially reversed the increase in visceral fat and the muscle insulin resistance, while completely normalizing muscle TG. Restricting intake of the high-fat diet to 75% of ad libitum completely prevented the increase in visceral fat and muscle insulin resistance. Maximally insulin-stimulated glucose transport was negatively correlated with visceral fat mass ( P < 0.001) in both the soleus and epitrochlearis muscles and with muscle TG concentration in the soleus ( P < 0.05) but not in the epitrochlearis. Thus we were unable to dissociate the increase in visceral fat from muscle insulin resistance using a variety of approaches. These results support the hypothesis that an increase in visceral fat is associated with development of muscle insulin resistance.

scholarly journals The effect of dietary fat on lipogenesis in mammary gland and liver from lactating and virgin mice

1969 ◽  
Vol 115 (4) ◽  
pp. 807-815 ◽  
Author(s):  
Stuart Smith ◽  
Harriet T. Gagné ◽  
Dorothy R. Pitelka ◽  
S. Abraham
Keyword(s):  
Mammary Gland ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Corn Oil ◽  
Acid Synthesis ◽  
High Fat ◽  
C3h Mice ◽  
Parenchymal Cells

1. Virgin and lactating C3H mice maintained on laboratory chow were transferred to a high-fat (15% corn oil) or a fat-free diet 3 days before being killed. 2. The linoleate content of liver, mammary gland and milk was decreased in lactating mice given the fat-free diet but was increased in those fed on the high-fat diet. Changes in linoleate content and mammary gland followed a similar but much less marked trend in virgin animals. 3. Hepatic fatty acid synthesis in lactating and virgin mice fed on the fat-free diet was higher than in corresponding animals fed on either the chow or the high-fat diet. The lipogenic capacity of livers from mice fed on either the chow or the high-fat diet was greater in lactating than in virgin animals. These changes in hepatic lipogenic capacity were accompanied by alterations in the specific activities of certain enzymes involved in fat synthesis. 4. Mammary gland from virgin and lactating animals showed no such adaptation to dietary fat. Results indicate that fatty acid synthesis in neither mammary-gland parenchymal cells nor mammary-gland adipose cells can be influenced by dietary fat in the same way as in the hepatocyte.

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.

scholarly journals Dietary fat and corticosterone levels are contributing factors to meal anticipation

2016 ◽  
Vol 310 (8) ◽  
pp. R711-R723 ◽  
Author(s):  
Sara Namvar ◽  
Amy Gyte ◽  
Mark Denn ◽  
Brendan Leighton ◽  
Hugh D. Piggins
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Content ◽  
High Fat ◽  
Contributing Factors ◽  
Low Fat ◽  
Restricted Access ◽  
Fos Expression ◽  
Fat Feeding

Daily restricted access to food leads to the development of food anticipatory activity and metabolism, which depends upon an as yet unidentified food-entrainable oscillator(s). A premeal anticipatory peak in circulating hormones, including corticosterone is also elicited by daily restricted feeding. High-fat feeding is associated with elevated levels of corticosterone with disrupted circadian rhythms and a failure to develop robust meal anticipation. It is not clear whether the disrupted corticosterone rhythm, resulting from high-fat feeding contributes to attenuated meal anticipation in high-fat fed rats. Our aim was to better characterize meal anticipation in rats fed a low- or high-fat diet, and to better understand the role of corticosterone in this process. To this end, we utilized behavioral observations, hypothalamic c-Fos expression, and indirect calorimetry to assess meal entrainment. We also used the glucocorticoid receptor antagonist, RU486, to dissect out the role of corticosterone in meal anticipation in rats given daily access to a meal with different fat content. Restricted access to a low-fat diet led to robust meal anticipation, as well as entrainment of hypothalamic c-Fos expression, metabolism, and circulating corticosterone. These measures were significantly attenuated in response to a high-fat diet, and animals on this diet exhibited a postanticipatory rise in corticosterone. Interestingly, antagonism of glucocorticoid activity using RU486 attenuated meal anticipation in low-fat fed rats, but promoted meal anticipation in high-fat-fed rats. These findings suggest an important role for corticosterone in the regulation of meal anticipation in a manner dependent upon dietary fat content.

scholarly journals High fat diet induces microbiota-dependent silencing of enteroendocrine cells

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Lihua Ye ◽  
Olaf Mueller ◽  
Jennifer Bagwell ◽  
Michel Bagnat ◽  
Rodger A Liddle ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Experimental System ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Sensory Cells ◽  
High Fat ◽  
Fat Feeding

Enteroendocrine cells (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient information. Consumption of dietary fat contributes to metabolic disorders, but EEC adaptations to high fat feeding were unknown. Here, we established a new experimental system to directly investigate EEC activity in vivo using a zebrafish reporter of EEC calcium signaling. Our results reveal that high fat feeding alters EEC morphology and converts them into a nutrient insensitive state that is coupled to endoplasmic reticulum (ER) stress. We called this novel adaptation 'EEC silencing'. Gnotobiotic studies revealed that germ-free zebrafish are resistant to high fat diet induced EEC silencing. High fat feeding altered gut microbiota composition including enrichment of Acinetobacter bacteria, and we identified an Acinetobacter strain sufficient to induce EEC silencing. These results establish a new mechanism by which dietary fat and gut microbiota modulate EEC nutrient sensing and signaling.

scholarly journals High fat diet induces microbiota-dependent silencing of enteroendocrine cells

2019 ◽  
Author(s):  
Lihua Ye ◽  
Olaf Mueller ◽  
Jennifer Bagwell ◽  
Michel Bagnat ◽  
Rodger A. Liddle ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Experimental System ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Sensory Cells ◽  
High Fat ◽  
Fat Feeding

ABSTRACTEnteroendocrine cells (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient information. Consumption of dietary fat contributes to metabolic disorders, but EEC adaptations to high fat feeding were unknown. Here, we established a new experimental system to directly investigate EEC activity in vivo using a zebrafish reporter of EEC calcium signaling. Our results reveal that high fat feeding alters EEC morphology and converts them into a nutrient insensitive state that is coupled to endoplasmic reticulum (ER) stress. We called this novel adaptation “EEC silencing”. Gnotobiotic studies revealed that germ-free zebrafish are resistant to high fat diet induced EEC silencing. High fat feeding altered gut microbiota composition including enrichment ofAcinetobacterspecies, and we identified anAcinetobacterstrain sufficient to induce EEC silencing. These results establish a new mechanism by which dietary fat and gut microbiota modulate EEC nutrient sensing and signaling.

Mechanism of fat-induced hepatic gluconeogenesis: effect of metformin

2001 ◽  
Vol 281 (2) ◽  
pp. E275-E282 ◽  
Author(s):  
Shaoming Song ◽  
Sofianos Andrikopoulos ◽  
Christine Filippis ◽  
Anne W. Thorburn ◽  
David Khan ◽  
...  
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Hepatic Insulin Resistance ◽  
High Fat ◽  
Protein Levels ◽  
Fructose 1,6 Bisphosphatase ◽  
Endogenous Glucose ◽  
Fat Feeding

High-fat feeding has been shown to cause hepatic insulin resistance. The aims of this study were to investigate the biochemical steps responsible for enhanced gluconeogenesis as a result of increased dietary fat intake and the site or sites at which the antihyperglycemic agent metformin acts to inhibit this process. Male Hooded Wistar rats were fed either a standard chow diet (5% fat by weight) or a high-fat diet (60% fat by weight) for 14 days with or without metformin. Total endogenous glucose production and gluconeogenesis were determined using [6-3H]glucose and [U-14C]alanine, respectively. Gluconeogenic enzyme activity and, where appropriate, protein and mRNA levels were measured in liver tissues. The high-fat diet increased endogenous glucose production (21.9 ± 4.4 vs. 32.2 ± 4.8 μmol · kg−1 · min−1, P < 0.05) and alanine gluconeogenesis (4.5 ± 0.9 vs. 9.6 ± 1.9 μmol · kg−1 · min−1, P < 0.05). Metformin reduced both endogenous glucose production (32.2 ± 4.8 vs. 16.1 ± 2.1 μmol · kg−1 · min−1, P < 0.05) and alanine gluconeogenesis (9.6 ± 1.9 vs. 4.7 ± 0.8 μmol · kg−1 · min−1, P < 0.05) after high-fat feeding. These changes were reflected in liver fructose-1,6-bisphosphatase protein levels (4.5 ± 0.9 vs. 9.6 ± 1.9 arbitrary units, P < 0.05 chow vs. high-fat feeding; 9.5 ± 1.9 vs. 4.7 ± 0.8 arbitrary units, P < 0.05 high fat fed in the absence vs. presence of metformin) but not in changes to the activity of other gluconeogenic enzymes. There was a significant positive correlation between alanine gluconeogenesis and fructose-1,6-bisphosphatase protein levels ( r = 0.56, P < 0.05). Therefore, excess supply of dietary fat stimulates alanine gluconeogenesis via an increase in fructose-1,6-bisphosphatase protein levels. Metformin predominantly inhibits alanine gluconeogenesis by preventing the fat-induced changes in fructose-1,6-bisphosphatase levels.

scholarly journals Regulation of plasma leptin in mice: influence of age, high-fat diet, and fasting

1997 ◽  
Vol 273 (1) ◽  
pp. R113-R120 ◽  
Author(s):  
B. Ahren ◽  
S. Mansson ◽  
R. L. Gingerich ◽  
P. J. Havel
Keyword(s):  
Body Weight ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Age Groups ◽  
Fat Content ◽  
High Fat ◽  
Background Strain ◽  
Plasma Leptin

Mechanisms regulating circulating leptin are incompletely understood. We developed a radioimmunoassay for mouse leptin to examine the influence of age, dietary fat content, and fasting on plasma concentrations of leptin in the background strain for the ob/ob mouse, the C57BL/6J mouse. Plasma leptin increased with age [5.3 +/- 0.6 ng/ml at 2 mo (n = 23) vs. 14.2 +/- 1.6 ng/ml at 11 mo (n = 15), P < 0.001]. Across all age groups (2-11 mo, n = 160), log plasma leptin correlated with body weight (r = 0.68, P < 0.0001), plasma insulin (r = 0.38, P < 0.001), and amount of intra-abdominal fat (r = 0.90, P < 0.001), as revealed by magnetic resonance imaging. Plasma leptin was increased by a high-fat diet (58% fat for 10 mo) and reduced by fasting for 48 h. The reduction of plasma leptin was correlated with the reduction of plasma insulin (r = 0.43, P = 0.012) but not with the initial body weight or the change in body weight. Moreover, the reduction in plasma leptin by fasting was impaired by high-fat diet. Thus plasma leptin in C57BL/6J mice 1) increases with age or a high-fat diet; 2) correlates with body weight, fat content, and plasma insulin; and 3) is reduced during fasting by an action inhibited by high-fat diet and related to changes of plasma insulin.

Impact of graded maternal dietary fat content on offspring susceptibility to high‐fat diet in mice

Obesity ◽  
2021 ◽  
Vol 29 (12) ◽  
pp. 2055-2067
Author(s):  
Yi Huang ◽  
Jazmin Osorio Mendoza ◽  
Min Li ◽  
Zengguang Jin ◽  
Baoguo Li ◽  
...  
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Content ◽  
High Fat

scholarly journals Impact of Dietary Fat on the Progression of Liver Fibrosis: Lessons from Animal and Cell Studies

2021 ◽  
Vol 22 (19) ◽  
pp. 10303
Author(s):  
Fangping Jia ◽  
Xiao Hu ◽  
Takefumi Kimura ◽  
Naoki Tanaka
Keyword(s):  
Fatty Acid ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Core Gene ◽  
High Fat ◽  
Virus Core ◽  
Liver Fibrogenesis ◽  
Isocaloric Diets

Previous studies have revealed that a high-fat diet is one of the key contributors to the progression of liver fibrosis, and increasing studies are devoted to analyzing the different influences of diverse fat sources on the progression of non-alcoholic steatohepatitis. When we treated three types of isocaloric diets that are rich in cholesterol, saturated fatty acid (SFA) and trans fatty acid (TFA) with hepatitis C virus core gene transgenic mice that spontaneously developed hepatic steatosis without apparent fibrosis, TFA and cholesterol-rich diet, but not SFA-rich diet, displayed distinct hepatic fibrosis. This review summarizes the recent advances in animal and cell studies regarding the effects of these three types of fat on liver fibrogenesis.

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