Chronic high-fat diet increases acute neuroendocrine stress response independently of prenatal dexamethasone treatment in male rats

ObjectiveIntrauterine growth restriction (IUGR) has been associated with metabolic disorders later in life such as obesity and diabetes as well as psychiatric disorders such as depression and schizophrenia. Therefore, we wanted to investigate whether behavioural, metabolic or neuroendocrine abnormalities could be provoked or exacerbated by a high-fat diet (HFD) in an experimental model of IUGR.MethodsPregnant dams were exposed to dexamethasone (DEX) in the third gestational week to induce IUGR. Late adolescent male offspring of DEX- and vehicle-treated dams were then fed a HFD or standard chow for 8 weeks and subjected to a variety of assessments.ResultsOnly diet affected the hypothalamus-pituitary-adrenal (HPA) axis stress response, as HFD doubled the observed corticosterone levels following acute restraint. HFD and prenatal DEX exposure concomitantly exacerbated depressive-like behaviour in the forced swim test, even though no interaction was seen. Prenatal DEX treatment tended to increase the basal acoustic startle response (ASR), while an interaction between HFD and DEX was present in the ASR pre-pulse inhibition suggestive of fundamental changes in neuronal gating mechanisms. Metabolic parameters were only affected by diet, as HFD increased fasting glucose and insulin levels.ConclusionWe conclude that chronic HFD may be more important in programming of the HPA axis stress responsiveness than an adverse foetal environment and therefore potentially implies an increased risk for developing psychiatric and metabolic disease.

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00500.2006 ◽

2007 ◽

Vol 293 (1) ◽

pp. E31-E41 ◽

Cited By ~ 90

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.

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Effects of high-fat diet-induced obesity and diabetes on Kiss1 and GPR54 expression in the hypothalamic–pituitary–gonadal (HPG) axis and peripheral organs (fat, pancreas and liver) in male rats

Neuropeptides ◽

10.1016/j.npep.2016.01.005 ◽

2016 ◽

Vol 56 ◽

pp. 41-49 ◽

Cited By ~ 28

Author(s):

M. Dudek ◽

P.A. Kołodziejski ◽

E. Pruszyńska-Oszmałek ◽

M. Sassek ◽

K. Ziarniak ◽

...

Keyword(s):

High Fat Diet ◽

Male Rats ◽

High Fat ◽

Hpg Axis ◽

Peripheral Organs ◽

Diet Induced Obesity ◽

Obesity And Diabetes

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1997.273.6.e1168 ◽

1997 ◽

Vol 273 (6) ◽

pp. E1168-E1177 ◽

Cited By ~ 43

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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Effect of Aerobic Training and High-fat Diet on Enos and Ros in Testicular Tissue of Juvenile Male Rats

Jundishapur Journal of Medical Sciences ◽

10.32598/jsmj.20.3.2045 ◽

2021 ◽

Vol 20 (3) ◽

pp. 280-289

Author(s):

Parisa Norouzzadeh ◽

◽

Roghayeh Pouzesh Jadidi ◽

Keyword(s):

Aerobic Exercise ◽

High Fat Diet ◽

Aerobic Training ◽

Testicular Tissue ◽

Normal Diet ◽

Male Rats ◽

Adolescent Male ◽

Male Mice ◽

High Fat ◽

Diet Control

Background and Objectives: This study aimed to determine the effect of a course of aerobic exercise with a high-fat diet on eNOS and ROS in testicular tissue of adolescent male rats. Subjects and Methods A total of 40 adolescent male rats (30 days old) were randomized in the following groups: normal diet control, normal diet training, high fat diet control, and high-fat diet training. The high-fat diet rats were under a high-fat regimen (5.817 kcal/g) for 30 days, and then a normal fat diet (3.801 kcal/g) was continued after the 60th day of birth. Aerobic training was conducted for four weeks included three training sessions from the 70th to 98th days of life. Results The results showed that the amount of ROS in the testicular tissue of male mice was higher only in the high-fat diet group. Also, there was no significant difference between the groups regarding eNOS testicular tissue in male mice. Conclusion A high-fat diet increases the production of reactive oxygen species in testicular tissue and is not affected by aerobic exercise. Also, neither exercise nor a high-fat diet had any effect on testicular eNOS. However, due to the limitations of this study and no evidence in this field, further studies are needed on cell phenotype, sperm fate, and identification of pathways involved in the occurrence of oxidative stress and subsequent effects of eNOS activation in testicular tissue in response to exercise and obesity.

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Impact of high-fat diet and antioxidant supplement on mitochondrial functions and gene transcripts in rat muscle

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00554.2001 ◽

2002 ◽

Vol 282 (5) ◽

pp. E1055-E1061 ◽

Cited By ~ 84

Author(s):

R. Sreekumar ◽

J. Unnikrishnan ◽

A. Fu ◽

J. Nygren ◽

K. R. Short ◽

...

Keyword(s):

Skeletal Muscle ◽

Free Radical ◽

Stress Response ◽

High Fat Diet ◽

Male Rats ◽

High Fat ◽

Antioxidant Supplementation ◽

Transcript Levels ◽

Atp Production ◽

Mitochondrial Functions

High-fat diets are reported to increase oxidative stress in a variety of tissues, whereas antioxidant supplementation prevents many diseases attributed to high-fat diet. Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage. We hypothesized that the effects of a high-fat diet on skeletal muscle DNA functions would be attenuated or partially reversed by antioxidant supplementation. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle from male rats after feeding one of three diets (control, high-fat diet with or without antioxidants) for 36 wk. The high-fat diet altered transcript levels of 18 genes of 800 surveyed compared with the control-fed rats. Alterations included reduced expression of genes involved in free-radical scavenging and tissue development and increased expression of stress response and signal transduction genes. The magnitude of these alterations due to high-fat diet was reduced by antioxidant supplementation. Real-time PCR measurements confirmed the changes in transcript levels of cytochrome c oxidase subunit III and superoxide dismutase-1 and -2 noted by microarray approach. Mitochondrial ATP production was unaltered by dietary changes or antioxidant supplemention. It is concluded that the high-fat diet increases the transcription of genes involved in stress response but reduces those of free-radical scavenger enzymes, resulting in reduced DNA repair/metabolism (increased DNA damage). Antioxidants partially prevent these changes. Mitochondrial functions in skeletal muscle remain unaltered by the dietary intervention due to many adaptive changes in gene transcription.

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The Effects of Brain Serotonin Deficiency on Responses to High Fat Diet in Female Mice

Frontiers in Neuroscience ◽

10.3389/fnins.2021.683103 ◽

2021 ◽

Vol 15 ◽

Author(s):

Shama N. Huq ◽

Allison K. Warner ◽

Kerry Buckhaults ◽

Benjamin D. Sachs

Keyword(s):

High Fat Diet ◽

Tryptophan Hydroxylase ◽

Forced Swim Test ◽

Brain Serotonin ◽

Dependent Manner ◽

Depression And Anxiety ◽

High Fat ◽

Anxiogenic Effect ◽

Increased Risk ◽

The Impact

Clinical studies have reported an increased risk of depression and anxiety disorders among individuals who are obese, and women are more likely than men to suffer from depression, anxiety, and obesity. However, the effects of obesity-promoting diets on depression- and anxiety-like behavior remain controversial. A recent study from our group used the tryptophan hydroxylase 2 (R439H) knock-in mouse line to evaluate the impact of genetic brain serotonin (5-HT) deficiency on behavioral responses to high fat diet (HFD) in male mice. That study indicated that chronic exposure to HFD induced pro-anxiety-like effects in the open field test and antidepressant-like effects in the forced swim test in wild-type males. Interestingly, the antidepressant-like effect of HFD, but not the anxiogenic effect, was blocked by brain 5-HT deficiency in males. The current work sought to repeat these studies in females. Our new data suggest that females are less susceptible than males to HFD-induced weight gain and HFD-induced alterations in behavior. In addition, the effects of chronic HFD on the expression of inflammation-related genes in the hippocampus were markedly different in females than we had previously reported in males, and HFD was shown to impact the expression of several inflammation-related genes in a genotype-dependent manner. Together, our findings highlight the importance of brain 5-HT and sex in regulating behavioral and molecular responses to HFD. Our results may have important implications for our understanding of the clinically observed sex differences in the consequences of obesity.

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Role of glucocorticoid signaling in exercise-associated changes in high-fat diet preference in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00288.2019 ◽

2020 ◽

Vol 318 (3) ◽

pp. R515-R528 ◽

Cited By ~ 1

Author(s):

Tiffany Y. Yang ◽

Jennie C. Gardner ◽

Zijun Gao ◽

Yuan-Xiang Pan ◽

Nu-Chu Liang

Keyword(s):

Sex Differences ◽

Hpa Axis ◽

High Fat Diet ◽

Wheel Running ◽

Expression Profiles ◽

Male Rats ◽

Diet Choice ◽

High Fat ◽

Diet Preference

The simultaneous introduction of wheel running (WR) and diet choice (high-carbohydrate chow vs. high-fat diet) results in sex-specific diet choice patterns in rats. WR induces a high-fat (HF) diet avoidance, and such avoidance persists in the majority of males, but not females, throughout a 2-wk period. Exercise is a physiological stressor that activates the hypothalamic-pituitary-adrenal (HPA) axis and stimulates glucocorticoid (GC) release, which can alter dietary preferences. Here, we examined the role of the HPA axis and GC signaling in mediating exercise-induced changes in diet preference and the associated neurobiological adaptations that may underlie sex differences in diet choice patterns. Experiment 1 revealed that adrenalectomy did not significantly alter the initiation and persistence of running-induced HF diet avoidance in male rats. Experiment 2 showed that acute WR resulted in greater neural activation than chronic WR in the medial prefrontal (mPFC) and insular cortices (IC) in male rats. Experiment 3 revealed sex differences in the molecular adaptation to exercise and diet preference. First, exercise increased gene expression of fkbp5 in the mPFC, IC, and hippocampus of WR females but had limited influence in males. Second, male and female WR rats that reversed or maintained HF diet avoidance showed distinct sex- and HF diet preference-dependent expression profiles of genes involved in cortical GC signaling (e.g., nr3c1, nr3c2, and src1). Taken together, our results suggest sex differences in region-specific neural adaptations may underlie sex differences in diet preference and the health benefits from exercise.

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Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642518 ◽

1994 ◽

Vol 71 (06) ◽

pp. 755-758 ◽

Cited By ~ 46

Author(s):

E M Bladbjerg ◽

P Marckmann ◽

B Sandström ◽

J Jespersen

Keyword(s):

High Fat Diet ◽

Fat Content ◽

Factor Vii ◽

Amidolytic Activity ◽

High Fat ◽

Low Fat Diet ◽

Increased Risk ◽

Coagulant Activity ◽

High Fat Diets ◽

Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

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