scholarly journals The Role of High-Fat Diets in Exacerbating Cognitive Deficits After Traumatic Brain Injury

2020 ◽  
Author(s):  
Michelle A Frankot
Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 636
Author(s):  
Germán Domínguez-Vías ◽  
Ana Belén Segarra ◽  
Manuel Ramírez-Sánchez ◽  
Isabel Prieto

High-fat diets (HFD) have been widely associated with an increased risk of metabolic disorders and overweight. However, a high intake of sources that are rich in monounsaturated fatty acids has been suggested as a dietary agent that is able to positively influence energy metabolism and vascular function. The main objective of this study was to analyze the role of dietary fats on hepatic peptidases activities and metabolic disorders. Three diets: standard (S), HFD supplemented with virgin olive oil (VOO), and HFD supplemented with butter plus cholesterol (Bch), were administered over six months to male Wistar rats. Plasma and liver samples were collected for clinical biochemistry and aminopeptidase activities (AP) analysis. The expression of inducible nitric oxide synthase (iNOS) was also determined by Western blot in liver samples. The diet supplement with VOO did not induce obesity, in contrast to the Bch group. Though the VOO diet increased the time that was needed to return to the basal levels of plasma glucose, the fasting insulin/glucose ratio and HOMA2-%B index (a homeostasis model index of insulin secretion and valuation of β-cell usefulness (% β-cell secretion)) were improved. An increase of hepatic membrane-bound dipeptidyl-peptidase 4 (DPP4) activity was found only in VOO rats, even if no differences in fasting plasma glucagon-like peptide 1 (GLP-1) were obtained. Both HFDs induced changes in hepatic pyroglutamyl-AP in the soluble fraction, but only the Bch diet increased the soluble tyrosyl-AP. Angiotensinase activities that are implicated in the metabolism of angiotensin II (AngII) to AngIV increased in the VOO diet, which was in agreement with the higher activity of insulin-regulated-AP (IRAP) in this group. Otherwise, the diet that was enriched with butter increased soluble gamma-glutamyl transferase (GGT) and Leucyl-AP, iNOS expression in the liver, and plasma NO. In summary, VOO increased the hepatic activity of AP that were related to glucose metabolism (DPP4, angiotensinases, and IRAP). However, the Bch diet increased activities that are implicated in the control of food intake (Tyrosine-AP), the index of hepatic damage (Leucine-AP and GGT), and the expression of hepatic iNOS and plasma NO. Taken together, these results support that the source of fat in the diet affects several peptidases activities in the liver, which could be related to alterations in feeding behavior and glucose metabolism.


2014 ◽  
Vol 16 (3) ◽  
pp. 307-320 ◽  

Obesity is now epidemic worldwide. Beyond associated diseases such as diabetes, obesity is linked to neuropsychiatric disorders such as depression. Alarmingly maternal obesity and high-fat diet consumption during gestation/lactation may "program" offspring longterm for increased obesity themselves, along with increased vulnerability to mood disorders. We review the evidence that programming of brain and behavior by perinatal diet is propagated by inflammatory mechanisms, as obesity and high-fat diets are independently associated with exaggerated systemic levels of inflammatory mediators. Due to the recognized dual role of these immune molecules (eg, interleukin [IL]-6, 11-1β) in placental function and brain development, any disruption of their delicate balance with growth factors or neurotransmitters (eg, serotonin) by inflammation early in life can permanently alter the trajectory of fetal brain development. Finally, epigenetic regulation of inflammatory pathways is a likely candidate for persistent changes in metabolic and brain function as a consequence of the perinatal environment.


2000 ◽  
Vol 84 (4) ◽  
pp. 417-427 ◽  
Author(s):  
Patrick Schrauwen ◽  
Klaas R. Westerterp

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.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Marwa El-Hindawy ◽  
Choon Young Kim ◽  
Bruce Hamaker

Abstract Objectives Our laboratory has recently shown that slowly digestible starch (SDS) that locationally digests to the ileum activates the gut-brain axis and reduces food intake in obese animals. Glucagon-like peptide-1 (GLP-1), oxyntomodulin (OXM), and peptide YY (PYY) are the main appetite-suppressing (anorexigenic) peptides of the intestinal enterendocrine L-cells that regulate postprandial insulin levels and satiety signals. We investigated the in vitro L-cell chemosensation of α-amylase starch digestion products, named maltooligosaccharides (MOS), and using SDS to deliver MOS in vivo. Methods Mouse (STC-1) and human (NCI-H716) cells were used to test chemosensation response and release of GLP-1, OXM and PYY after MOS treatment. Differential gene expression and comparable global protein profiling of STC-1 cell treated with MOS was tested using RNA sequencing and LC-MS/MS analysis. Alginate-entrapped SDS microspheres that digest distally into the ileum were used to examine the role of SDS in the intervention and prevention of obesity in C57BL/6 J obese and lean mice, respectively. Body weight, food intake and body composition were monitored periodically. Results MOS exhibited significantly higher stimulatory effect on GLP-1 and OXM secretion in mouse and human L-cells, respectively, compared to glucose. Multi-omics analysis showed that MOS induced exocytosis of GLP-1- and OXM-containing vesicles and did not induce positive regulation of the proglucagon gene suggesting that secretion, but not synthesis, of the proglucagon gene products was enhanced by MOS. In vivo Results showed that 20% SDS in low-fat diets significantly improved weight loss and food intake reduction in obese mice. Similarly, 15% SDS in high-fat diets showed significant reduction in body fat %, increase in lean body mass, and considerable reduction in weight gain rate and food intake in lean mice fed on high-fat diets. Conclusions We propose several insights into L-cell sensation of dietary starch-degraded MOS delivered by the consumption of slowly digestible starch. MOS exhibit unique influences on L-cell sensitivity and gut hormone productivity. The intricate role of dietary carbohydrates on gut physiological response, related to satiety and food intake could be a new approach for design of foods for obesity prevention. Funding Sources Whistler Center for Carbohydrate Research, Purdue University. Supporting Tables, Images and/or Graphs


2019 ◽  
Vol 80 (1) ◽  
Author(s):  
Atef Abdel-Moneem Ali ◽  
Anwar Mansour ◽  
El-sayed Abd-elkhalik Hassanine ◽  
Amal Hamed Abdel-Razek ◽  
Heba Ali Hassan Mahmoud

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