scholarly journals No effect of a high-fat diet on promotion of sex hormone-induced prostate and mammary carcinogenesis in the Noble rat model

2002 ◽  
Vol 88 (4) ◽  
pp. 399-409 ◽  
Author(s):  
G. Leung ◽  
I. F. F. Benzie ◽  
A. Cheung ◽  
S. W. Tsao ◽  
Y. C. Wong
Keyword(s):  
Weight Gain ◽  
Rat Model ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Mammary Cancer ◽  
Mammary Carcinogenesis ◽  
Sex Hormone ◽  
Female Rats ◽  
Male Rats ◽  
High Fat

Results of international correlation and migrant studies suggest that dietary fat promotes carcinogenesis in hormone-sensitive sites, but this is disputed. In the present study, we used a Noble rat model of sex hormone-induced cancers to examine the effect of a high-fat diet on the incidence and latency of prostate and mammary cancer in male (n 139) and female (n 72) animals respectively. We also measured α-tocopherol levels in female breast tissue to determine whether a high intake of polyunsaturated fatty acids depletes antioxidant defence in target tissues, providing a possible potentiating mechanism for carcinogenesis. Results showed a very high incidence of hormone-induced adenocarcinomas of prostate and mammary gland, irrespective of diet. There was no difference in the pattern of carcinogenesis in different prostatic locations, weight of the prostate, or weight gain between male rats on the high-fat diet compared with the control (standard, low-fat) diet. In female rats, the incidence of mammary cancer and the body-weight gain were the same in both dietary groups, and breast α-tocopherol was also unaffected by dietary fat intake. Our present results are supportive of recent cohort studies that reported no significant association between intake of fat and the development of human prostate and breast cancer, and do not support a role for dietary fat in promoting sex hormone-induced prostate and mammary carcinogenesis.

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

2007 ◽  
Vol 293 (1) ◽  
pp. E31-E41 ◽  
Author(s):  
Robert C. Noland ◽  
John P. Thyfault ◽  
Sarah T. Henes ◽  
Brian R. Whitfield ◽  
Tracey L. Woodlief ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Gain ◽  
High Fat Diet ◽  
Oxidative Capacity ◽  
Male Rats ◽  
High Fat ◽  
Endurance Running ◽  
Muscle Oxidative Capacity ◽  
Obesity And Diabetes

Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.

scholarly journals High-fat diet-induced hypertension is associated with a proinflammatory T cell profile in male and female Dahl salt-sensitive rats

2018 ◽  
Vol 315 (6) ◽  
pp. H1713-H1723 ◽  
Author(s):  
Lia E. Taylor ◽  
Ellen E. Gillis ◽  
Jacqueline B. Musall ◽  
Babak Baban ◽  
Jennifer C. Sullivan
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
High Fat Diet ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Male And Female ◽  
The Impact ◽  
Cell Profile

Evidence supports a sex difference in the impact of a high-fat diet (HFD) on cardiovascular outcomes, with male experimental animals exhibiting greater increases in blood pressure (BP) than female experimental animals. The immune system has been implicated in HFD-induced increases in BP, and there is a sex difference in T-cell activation in hypertension. The goal of this study was to determine the impact of HFD on BP and aortic and renal T cell profiles in male and female Dahl salt-sensitive (DSS) rats. We hypothesized that male DSS rats would have greater increases in BP and T cell infiltration in response to a HFD compared with female DSS rats. BP was measured by tail-cuff plethysmography, and aortic and renal T cells were assessed by flow cytometric analysis in male and female DSS rats on a normal-fat diet (NFD) or HFD from 12 to 16 wk of age. Four weeks of HFD increased BP in male and female DSS rats to a similar degree. Increases in BP were accompanied by increased percentages of CD4+ T cells and T helper (Th)17 cells in both sexes, although male rats had more proinflammatory T cells. Percentages of renal CD3+ and CD4+ T cells as well as Th17 cells were increased in both sexes by the HFD, although the increase in CD3+ T cells was greater in male rats. HFD also decreased the percentage of aortic and renal regulatory T cells in both sexes, although female rats maintained more regulatory T cells than male rats regardless of diet. In conclusion, both male and female DSS rats exhibit BP sensitivity to a HFD; however, the mechanisms mediating HFD-induced increases in BP may be distinct as male rats exhibit greater increases in the percentage of proinflammatory T cells than female rats. NEW & NOTEWORTHY Our study demonstrates that male and female Dahl salt-sensitive rats exhibit similar increases in blood pressure to a high-fat diet and an increase in aortic and renal T cells. These results are in contrast to studies showing that female rats remain normotensive and/or upregulate regulatory T cells in response to hypertensive stimuli compared with male rats. Our data suggest that a 4-wk high-fat diet has sex-specific effects on the T cell profile in Dahl salt-sensitive rats.

scholarly journals Study on optimization and stability of a single dose streptozotocin-induced diabetic modeling in rats

2020 ◽  
Author(s):  
Yao Zhang ◽  
jiao Zhang ◽  
Ming Hong ◽  
Jingyi Huang ◽  
Rui Wang ◽  
...  
Keyword(s):  
Blood Glucose ◽  
High Fat Diet ◽  
Female Rats ◽  
Male Rats ◽  
Control Group ◽  
High Fat ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Sd Rats ◽  
Male And Female Rats

Abstract BackgroundOptimization of experimental conditions in streptozotocin induced diabetic model in Sprague Dawley (SD) rats to evaluate the stability of the model.MethodsMale and female SD rats were randomly divided into control group, STZ 45 group (STZ: 45 mg / kg), STZ 65 group (STZ: 65 mg / kg), STZ 85 group (STZ: 85 mg / kg), high fat diet with STZ 45 group (STZ: 45 mg / kg), high fat diet with STZ 65 group (STZ: 65 mg / kg), high fat diet with STZ 85 group (STZ: 85 mg / kg). N = 6 in each group. The changes of body weight and blood glucose were observed dynamically.ResultsThere was no significant difference in blood glucose or body weight between the STZ 45 group and the control group in both male and female rats, whether or not they were on a high-fat diet. However, there were significant differences in blood glucose between the high-dose STZ group and the control group in both male and female rats, regardless of whether the rats were on a high-fat diet or not (P < 0.05 or P < 0.01). Compared with the control group, there were significant differences in blood glucose levels (P < 0.05 or P < 0.01) and higher blood glucose levels in the male rats fed with the normal diet than that in those fed with the high-fat diet.ConclusionsIn this study, male rats fed with ordinary feed and injected STZ dose of 65 mg / kg were the most stable and ideal diabetic rat.

Trafficking of dietary fat in obesity-prone and obesity-resistant rats

2006 ◽  
Vol 291 (5) ◽  
pp. E1083-E1091 ◽  
Author(s):  
Matthew R. Jackman ◽  
Robert E. Kramer ◽  
Paul S. MacLean ◽  
Daniel H. Bessesen
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Tracer Uptake ◽  
Female Rats ◽  
Male Rats ◽  
Gi Tract ◽  
Feeding Tubes ◽  
Male And Female Rats ◽  
Gastric Feeding

The trafficking of dietary fat was assessed in obesity-prone (OP) and obesity-resistant (OR) male and female rats. Test meals containing [1-14C]palmitate were delivered through gastric feeding tubes while rats consumed a high-carbohydrate diet (HCD) or after 5 days of a high-fat diet (HFD). Over the subsequent 24 h, the appearance of 14C was followed in the GI tract, skeletal muscles (SM), liver, adipose tissues (AT), and expired CO2. There was no difference in the production of 14CO2 between OP and OR rats consuming a HCD. However, after 5 days on HFD, OR rats produced significantly more 14CO2 after the test meal than OP rats ( P < 0.001 females, P = 0.03 males). The differential oxidation of dietary fat between OP and OR rats on HFD was not due to differences in absorption but rather was associated with preferential disposition of tracer to AT in OP rats. Measurements of lipoprotein lipase in part explained increased tracer uptake by AT in OP rats but were not consistent with increased SM tracer uptake in OR rats. Surprisingly, female rats oxidized more tracer than male rats irrespective of phenotype or diet. These results are consistent with the notion that differences in the partitioning of dietary fat between storage in AT and oxidation in SM and liver that develop shortly after the introduction of a HFD may in part underlie the differential tendency for OR and OP rats to gain weight on this diet.

scholarly journals Macronutrient balances and obesity: the role of diet and physical activity

1999 ◽  
Vol 2 (3a) ◽  
pp. 341-347 ◽  
Author(s):  
Arne Astrup
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Physical Fitness ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Oxidation ◽  
Fat Content ◽  
High Fat

AbstractObservational cross-sectional and longitudinal studies suggest that a high fat diet and physical inactivity are independent risk factors for weight gain and obesity. Mechanistic and intervention studies support that fat possesses a lower satiating power than carbohydrate and protein, and a diet low in fat therefore decreases energy intake. The effect of dietary fat on energy balance is enhanced in susceptible subjects, particularly in sedentary individuals with a genetic predisposition to obesity who consume a high fat diet.Dietary carbohydrate promotes its own oxidation by an insulin-mediated stimulation of glucose oxidation. In contrast, high fat meals do not increase fat oxidation acutely. A sedentary life-style and low physical fitness cause a low muscular fat oxidation capacity, and the consumption of a high fat diet by these individuals promotes fat storage in a synergistic fashion.Ad libitum low fat diets cause weight loss proportional to pre-treatment body weight in a dose-dependent way, i.e. weight loss is correlated positively to the reduction in dietary fat content. Increased physical activity prevents relapse after weight loss and studies have shown that those who keep up a higher level of physical activity are more successful in maintaining the reduced body weight. In conclusion, important interactions exist between genetic make up, dietary fat and physical fitness, so that a low fitness level and susceptible genes reduce muscular fat oxidation capacity which may decrease the tolerance of dietary fat. Increasing daily physical activity and reducing dietary fat content may be more effective when combined than when separate in preventing weight gain and obesity.

scholarly journals Sex differences in gut microbiome in high-fat-diet fed rats.

2020 ◽  
Author(s):  
Ying Shi ◽  
Fangzhi Yue ◽  
Lin Xing ◽  
Shanyu Wu ◽  
Lin Wei ◽  
...  
Keyword(s):  
Sex Differences ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Normal Diet ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Alcoholic Fatty Liver

Abstract Background Sex differences in obesity and related metabolic diseases are well recognized, however, the mechanism has not been elucidated. Gut microbiota and its metabolites may play a vital role in the development of obesity and metabolic diseases. The aim of the present study was to investigate sex differences in gut microbiota and its metabolites in a high-fat-diet (HFD) obesity rats and identify microbiota genera potentially contributing to such differences in obesity and non-alcoholic fatty liver disease (NAFLD) susceptibility. Results Sprague–Dawley rats were divided into the following groups (seven animals per group): (1) male rats on a normal diet (MND), (2) male rats on HFD (MHFD), (3) female rats on a normal diet (FND), and (4) female rats on HFD (FHFD). HFD induced more body weight gain and fat storage in female rats, however, lower hepatic steatosis in FHFD than in MHFD rats was observed. When considering gut microbiota composition, FHFD rats had lower microbiome diversity than MHFD. A significant increase of Firmicutes phylum and Bilophila genus was detected in MHFD rats, as compared with FHFD, which showed increased relative abundance of Murimonas and Roseburia . Moreover, propionic and lauric acid levels were higher in FHFD than those in MHFD rats. Conclusion HFD induced sex-related alterations in gut microbiome and fatty acids. Furthermore, the genus Bilophila and Roseburia might contribute to sex differences observed in obesity and NAFLD susceptibility.

scholarly journals Effects of Diet-Induced Obesity on Hypothalamic Kisspeptin-Neurokinin-Dynorphin (KNDy) Neurons and Luteinizing Hormone Secretion in Sex Hormone-Primed Male and Female Rats

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A537-A537
Author(s):  
Shiori Minabe ◽  
Kinuyo Iwata ◽  
Hitoshi Ozawa
Keyword(s):  
Gene Expression ◽  
Luteinizing Hormone ◽  
High Fat Diet ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Neurokinin B ◽  
Male And Female ◽  
Male And Female Rats ◽  
Kndy Neurons

Abstract Metabolic stress resulting from a nutrient excess causes infertility in both sexes. Kisspeptin-neurokinin B-dynorphin (KNDy) neurons in the arcuate nucleus (ARC) have been suggested to be key players in reproduction via direct stimulation of gonadotropin-releasing hormone (GnRH) and subsequent gonadotropin release in mammalian species. In this study, we investigated the sex differences in the effects of a high-fat diet (HFD) on KNDy-associated gene expression in the ARC to determine the pathogenic mechanism underlying obesity-induced infertility. Wistar-Imamichi strain male and female rats (7 weeks of age) were fed either a standard diet (10% calories from fat) or high-fat diet (45% calories from fat) for 4 months. In male rats, the HFD caused a significant suppression of Kiss1(encoding kisspeptin), Tac3(encoding neurokinin B), and Pdyn(encoding dynorphin A) gene expression in the ARC, resulting in a decrease in plasma luteinizing hormone (LH) levels. In female rats, 58% of the HFD-fed female rats exhibited irregular estrous cycles, while the other rats showed regular cycles. LH pulses were found, and the numbers of ARC Kiss1-,Tac3-, and Pdyn-expressing cells were high in control animals and almost allHFD-fed female rats, but two out of 10 rats showed profound HFD-induced suppression of LH pulse frequency and reduction in these cells. No statistical differences in LH secretion or ARC KNDy gene expression were observed between HFD-fed and control female rats. Additionally, the number of Gnrh1-expressing cells in the preoptic area was comparable between the groups in both sexes. Our findings revealed that HFD-fed male rats showed KNDy-dependent infertility, while irregular menstruation was mainly induced by KNDy-independent pathways during the incipient stage of obese infertility in female rats. Taken together, hypothalamic kisspeptin neurons in male rats may be susceptible to HFD-induced obesity compared with those in female rats.

Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring

2018 ◽  
Vol 9 (3) ◽  
pp. 315-328 ◽  
Author(s):  
E. K. Zinkhan ◽  
B. Yu ◽  
C. W. Callaway ◽  
R. A. McKnight
Keyword(s):  
High Fat Diet ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Serum Corticosterone ◽  
Regular Diet ◽  
Intrauterine Growth ◽  
Rat Offspring

AbstractIntrauterine growth restriction (IUGR) and fetal exposure to a maternal high-fat diet (HFD) independently increase the risk of developing obesity in adulthood. Excess glucocorticoids increase obesity. We hypothesized that surgically induced IUGR combined with an HFD would increase adiposity and glucocorticoids more than in non-IUGR offspring combined with the same HFD, findings that would persist despite weaning to a regular diet. Non-IUGR (N) and IUGR (I) rat offspring from dams fed either regular rat chow (R) or an HFD (H) were weaned to either a regular rat chow or an HFD. For non-IUGR and IUGR rats, this study design resulted in three diet groups: offspring from dams fed a regular diet and weaned to a regular diet (NRR and IRR), offspring rats from dams fed an HFD and weaned to a regular diet (NHR and IHR) and offspring from dams fed an HFD and weaned to an HFD (NHH and IHH). Magnetic resonance imaging or fasting visceral and subcutaneous adipose tissue collection occurred at postnatal day 60. IHH male rats had greater adiposity than NHH males, findings that were only partly normalized by weaning to a regular chow. IHH male rats had a 10-fold increase in serum corticosterone levels. IHH female rats had increased adiposity and serum triglycerides. We conclude that IUGR combined with an HFD throughout life increased adiposity, glucocorticoids and triglycerides in a sex-specific manner. Our data suggest that one mechanism through which the perinatal environment programs increased adiposity in IHH male rats may be via increased systemic glucocorticoids.

Effects of combined glucocorticoid/mineralocorticoid receptor modulation (CORT118335) on energy balance, adiposity, and lipid metabolism in male rats

2019 ◽  
Vol 317 (2) ◽  
pp. E337-E349
Author(s):  
Elizabeth T. Nguyen ◽  
Sarah Berman ◽  
Joshua Streicher ◽  
Christina M. Estrada ◽  
Jody L. Caldwell ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
The Body ◽  
Male Rats ◽  
Chow Diet ◽  
High Fat ◽  
Receptor Modulation

Psychological stress and excess glucocorticoids are associated with metabolic and cardiovascular diseases. Glucocorticoids act primarily through mineralocorticoid (MR) and glucocorticoid receptors (GR), and compounds modulating these receptors show promise in mitigating metabolic and cardiovascular-related phenotypes. CORT118335 (GR/MR modulator) prevents high-fat diet-induced weight gain and adiposity in mice, but the ability of this compound to reverse obesity-related symptoms is unknown. Adult male rats were subcutaneously administered CORT118335 (3, 10, or 30 mg/kg) or vehicle once daily. A 5-day treatment with CORT118335 at 30 mg/kg induced weight loss in rats fed a chow diet by decreasing food intake. However, lower doses of the compound attenuated body weight gain primarily because of decreased calorific efficiency, as there were no significant differences in food intake compared with vehicle. Notably, the body weight effects of CORT118335 persisted during a 2-wk treatment hiatus, suggesting prolonged effects of the compound. To our knowledge, we are the first to demonstrate a sustained effect of combined GR/MR modulation on body weight gain. These findings suggest that CORT118335 may have long-lasting effects, likely due to GR/MR-induced transcriptional changes. Prolonged (18 days) treatment of CORT118335 (10 mg/kg) reversed body weight gain and adiposity in animals fed a high-fat diet for 13 wk. Surprisingly, this occurred despite a worsening of the lipid profile and glucose homeostasis as well as a disrupted diurnal corticosterone rhythm, suggesting GR agonistic effects in the periphery. We conclude that species and tissue-specific targeting may result in promising leads for exploiting the metabolically beneficial aspects of GR/MR modulation.

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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