Effects Of High-fat Consumption Research Articles

Sub Chronic effect of High fat consumption on heart rate variability and Nitric oxide (NO) in experimental rats: Protective role of Terminalia arjuna

Background: In the present study Albino wister rats displayed with increase in body weight, sympathetic activity and decreased parasympathetic function following a high fat consumption for a sub chronic period. Possible alterations of cardiac autonomic functions and molecular behaviour of nitric oxide were observed in the presence of ethanolic extract of Terminalia arjuna (ETA). Objectives: The study was aimed to find out impact of high fat diet on cardiac health in terms with HRV also through NO pathways alterations in experimental rats and to assess the cardio protective efficacy of Terminalia arjuna on hyperlipidemic rats. Methodology: Bark of Terminalia arjuna was extracted with 99% ethanol. Rats were grouped into four groups (n=6); Control as group 1 (20% fat); group 2 fed with (20% fat+ ETA 100 mg/kg/b w); group 3 fed with (30% fat) and group 4 fed with (30% fat + ETA 100mg/kg/b w). Body weight and percentage of body weight gain were calculated. Electrophysiological analysis(HRV and sympatho-vagal balance) were done. Biochemical assay was done to assess serum Nitric oxide levels(NO). ANOVA, Pearson’s correlation and multiple regression were done to analyze data. Results: Electrophysiological evaluation revealed altered sympatho-vagal balance in hyperlipidemic rats. Significant increase in sympathetic drive along with decrease in parasympathetic functions suggests cardiac autonomic dysfunction in rats fed with high fat. Subchronic supplementation of ethanolic extraction of Terminalia arjuna to hyperlipidemic rats showed significant beneficial effect on cardiac autonomic function. Significant negative correlation was observed between HRV and nitric oxide. Conclusion: Terminalia arjuna have exhibited its cardioprotective role in high fat fed rats by enhancing cardiac functions. Supplementation of ETA have shown important role in modulating autonomic control and in improving cardiovascular function. Probably polyphenolic compounds and flavonoids might have cardioprotective activity by rejuvenating action and free radical quenching actions.

Dietary Fatty Acids Sustain the Growth of the Human Gut Microbiota.

While a substantial amount of dietary fats escape absorption in the human small intestine and reach the colon, the ability of resident microbiota to utilize these dietary fats for growth has not been investigated in detail. In this study, we used an in vitro multivessel simulator system of the human colon to reveal that the human gut microbiota is able to utilize typically consumed dietary fatty acids to sustain growth. Gut microbiota adapted quickly to a macronutrient switch from a balanced Western diet-type medium to its variant lacking carbohydrates and proteins. We defined specific genera that increased in their abundances on the fats-only medium, including Alistipes, Bilophila, and several genera of the class Gammaproteobacteria In contrast, the abundances of well-known glycan and protein degraders, including Bacteroides, Clostridium, and Roseburia spp., were reduced under such conditions. The predicted prevalences of microbial genes coding for fatty acid degradation enzymes and anaerobic respiratory reductases were significantly increased in the fats-only environment, whereas the abundance of glycan degradation genes was diminished. These changes also resulted in lower microbial production of short-chain fatty acids and antioxidants. Our findings provide justification for the previously observed alterations in gut microbiota observed in human and animal studies of high-fat diets.IMPORTANCE Increased intake of fats in many developed countries has raised awareness of potentially harmful and beneficial effects of high fat consumption on human health. Some dietary fats escape digestion in the small intestine and reach the colon where they can be metabolized by gut microbiota. We show that human gut microbes are able to maintain a complex community when supplied with dietary fatty acids as the only nutrient and carbon sources. Such fatty acid-based growth leads to lower production of short-chain fatty acids and antioxidants by community members, which potentially have negative health consequences on the host.

A high fat diet alters metabolic and bioenergetic function in the brain: A magnetic resonance spectroscopy study

Diet-induced obesity and associated metabolic effects can lead to neurological dysfunction and increase the risk of developing Alzheimer's disease (AD) and Parkinson's disease (PD). Despite these risks, the effects of a high-fat diet on the central nervous system are not well understood. To better understand the mechanisms underlying the effects of high fat consumption on brain regions affected by AD and PD, we used proton magnetic resonance spectroscopy (1H-MRS) to measure neurochemicals in the hippocampus and striatum of rats fed a high fat diet vs. normal low fat chow. We detected lower concentrations of total creatine (tCr) and a lower glutamate-to-glutamine ratio in the hippocampus of high fat rats. Additional effects observed in the hippocampus of high fat rats included higher N-acetylaspartylglutamic acid (NAAG), and lower myo-inositol (mIns) and serine (Ser) concentrations. Post-mortem tissue analyses revealed lower phosphorylated AMP-activated protein kinase (pAMPK) in the striatum but not in the hippocampus of high fat rats. Hippocampal pAMPK levels correlated significantly with tCr, aspartate (Asp), phosphoethanolamine (PE), and taurine (Tau), indicating beneficial effects of AMPK activation on brain metabolic and energetic function, membrane turnover, and edema. A negative correlation between pAMPK and glucose (Glc) indicates a detrimental effect of brain Glc on cellular energy response. Overall, these changes indicate alterations in neurotransmission and in metabolic and bioenergetic function in the hippocampus and in the striatum of rats fed a high fat diet.

Exposure to common food additive carrageenan alone leads to fasting hyperglycemia and in combination with high fat diet exacerbates glucose intolerance and hyperlipidemia without effect on weight.

Aims. Major aims were to determine whether exposure to the commonly used food additive carrageenan could induce fasting hyperglycemia and could increase the effects of a high fat diet on glucose intolerance and dyslipidemia. Methods. C57BL/6J mice were exposed to either carrageenan, high fat diet, or the combination of high fat diet and carrageenan, or untreated, for one year. Effects on fasting blood glucose, glucose tolerance, lipid parameters, weight, glycogen stores, and inflammation were compared. Results. Exposure to carrageenan led to glucose intolerance by six days and produced elevated fasting blood glucose by 23 weeks. Effects of carrageenan on glucose tolerance were more severe than from high fat alone. Carrageenan in combination with high fat produced earlier onset of fasting hyperglycemia and higher glucose levels in glucose tolerance tests and exacerbated dyslipidemia. In contrast to high fat, carrageenan did not lead to weight gain. In hyperinsulinemic, euglycemic clamp studies, the carrageenan-exposed mice had higher early glucose levels and lower glucose infusion rate and longer interval to achieve the steady-state. Conclusions. Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption. Carrageenan may be useful as a nonobese model of diabetes in the mouse.

Effects of high-fat diet on insulin receptor function in rat hippocampus and the level of neuronal corticosterone

AimChronic consumption of a high-fat (HF) diet contributes to peripheral insulin resistance and elevated plasma corticosterone. However, the effect of HF consumption on the neurofunctional insulin receptors and neuronal corticosterone level is unclear. We tested the hypothesis that HF consumption can lead to peripheral insulin resistance, elevated neuronal corticosterone, and impaired neuronal responses to insulin. Main methodsMale Wistar rats were fed with normal diet or HF diet for 4, 8 or 12weeks. At the end of each dietary period, plasma was collected for investigating peripheral insulin resistance parameters and corticosterone. Brains were then rapidly removed for studying the function of neuronal insulin receptors (IRs) by extracellular recording in CA1 hippocampus, neuronal IR signaling by immunoblot technique and neuronal corticosterone. Key findingsElevated plasma corticosterone level was initially seen in 4-week HF-fed rats. Peripheral insulin resistance developed at 8-week HF-fed rats. However, the elevated neuronal corticosterone level was found at 12-week HF consumption. The neuronal IR response demonstrated by insulin-mediated long-term depression in CA1 hippocampus was diminished in 12-week HF-fed rats. The phosphorylation levels of neuronal IR, IR substrate 1 and Akt/PKB were decreased in 12-week HF-fed rats with no change in these proteins. There was a correlation among peripheral insulin resistance, neuronal stress (elevated neuronal corticosterone), and neuronal insulin resistance in HF group. SignificanceOur findings suggest that HF consumption can lead to the elevation of corticosterone and peripheral insulin resistance, which could contribute to neuronal insulin resistance and neuronal stress.

Ras may mediate mammary cancer promotion by high fat.

High fat consumption has been implicated as a risk factor for breast cancer. Experimental mammary carcinogenesis studies have demonstrated that the effect of high fat consumption is mainly exerted on the postinitiation stage of the disease process. We report data that have recalled in the formulation of a new hypothesis about the effect of dietary fat on mammary carcinogenesis, namely, that it promotes the development of a subpopulation of cells lacking a specific pathogenetic characteristic. In comparison with animals fed a low-fat diet, female Sprague-Dawley rats fed high-fat diets during the promotional stage developed significantly more (number and proportion) 1-methyl-1-nitrosourea-induced mammary adenocarcinomas that did not contain a codon 12 GGA-->GAA mutation in the c-Ha-ras protooncogene. The effect was independent of the types of fat fed, i.e., corn oil vs. fish oil. A model is presented to account for the preferential promotional effect of high fat consumption on 1-methyl-1-nitrosourea-initiated mammary epithelial cells. The hypothesis that the level of dietary fat consumed affects the proportion of mammary carcinomas that occur with a particular pathogenetic characteristic, in this case, the presence or absence of a Ha-ras point mutation, has important implications on the direction of future investigations concerning fat and cancer risk.