High-carbohydrate Diet Group Research Articles

Histological Analysis of Enamel Microstructure in Response to Dietary Habits: Comparative Study A cross Different Populations

Background: The protective role of enamel against physical and chemical injury is well documented. Despite being classified as connective tissue, with its composition and microstructure dominated by hydroxyapatite crystals it is the hardest in the human body Objective: The purpose of this study is to investigate the histological changes in enamel microstructure that occur when distinct populations follow different food habits. Study Design: This study employs a comparative cross-sectional design. Duration and Place of the Study: This study was conducted at Department of pathology Watim medical and dental college, Rawat , from 3rd June 2022 to 2nd May 2023. Material and Methods: A sum of 300 dental examples were acquired from members having a place with one or the other, High Carbohydrate Diet Group (n=95): people accounting their principle dietary consumption high-carb nourishments like grains/pay/aries and starches. High-Proteins Diet Group (n=108): participants who had the highest consumption of protein-rich foods, such as meat products, legumes and dairy. Mixed Diet Group (n=97): People with intermediate consumptions of carbohydrates, proteins and fats Subsequently, study participants were determined to best represent the two diet groups based on dietary surveys and medical histories. Results: In total, 300 participants are considered in this research, with the mean age of the group on HC totals 3.5 ± 1.3 years, HP group 3.4 ± 9.2 years, and MD group 3.6 ± 1.1 years. The gender distribution also shows similar characteristics, males are 55.8% in HC group, 46.3% in HP group, and 52.6% in MD group; females are 44.2%, 53.7%, and 47.4%, respectively. Concerning the age range, the major cluster is 26-35 years old and 36-45 years old cohorts, which proves the majority of the middle ages. Conclusion: Our results indicate that decomposition is a major factor affecting the surface morphology, structure and health of enamel.

Effects of Different Carbohydrate Content Diet on Gut Microbiota and Aortic Calcification in Diabetic Mice.

Vascular calcification is a major cause of cardiovascular accidents in patients with type 2 diabetes mellitus. This study aimed to investigate the impact of carbohydrates on gut microbiota and aortic calcification in diabetic ApoE-/- mice. The diabetic ApoE-/- mice were randomly divided into 4 groups: ketogenic diet group, low carbohydrate diet group, medium carbohydrate diet group, and high carbohydrate diet group. The mice were fed continuously for 6 months, with blood glucose, blood ketone and body weight monitored monthly. Lipid metabolism indicators and inflammatory factors were detected using ELISA. The intestinal barrier, atherosclerotic lesion areas, and vascular calcifications were analyzed based on their morphology. Gut microbiota was analyzed using 16S rRNA genes. We found that ketogenic diet played some roles improving glucose, lipid metabolism, and inflammation. Ketogenic diet could improve the intestinal barrier to some extent and increase intestinal bacteria. Compared to the other three groups, the relative abundance of genus Allobaculum, species Blautia producta and Clostridium Ramosum in the ketogenic diet group was significantly increased (P <0.05), which has protective effects in diabetic ApoE-/- mice. Ketogenic diet could delay the onset of aortic atherosclerosis, aortic calcification and improve intestinal barrier function in diabetic ApoE-/- mice.

Sequential Activations of ChREBP and SREBP1 Signals Regulate the High-Carbohydrate Diet-Induced Hepatic Lipid Deposition in Gibel Carp (Carassius gibelio).

The present study investigated the sequential regulation signals of high-carbohydrate diet (HCD)-induced hepatic lipid deposition in gibel carp (Carassius gibelio). Two isonitrogenous and isolipidic diets, containing 25% (normal carbohydrate diet, NCD) and 45% (HCD) corn starch, were formulated to feed gibel carp (14.82 ± 0.04 g) for 8 weeks. The experimental fish were sampled at 2nd, 4th, 6th, and 8th week. In HCD group, the hyperlipidemia and significant hepatic lipid deposition (oil red O area and triglyceride content) was found at 4th, 6th, and 8th week, while the significant hyperglycemia was found at 2nd, 4th, and 8th week, compared to NCD group (P < 0.05). HCD induced hepatic lipid deposition via increased hepatic lipogenesis (acc, fasn, and acly) but not decreased hepatic lipolysis (hsl and cpt1a). When compared with NCD group, HCD significantly elevated the hepatic sterol regulatory element binding proteins 1 (SREBP1) signals (positive hepatocytes and fluorescence intensity) at 4th, 6th, and 8th week (P < 0.05). The hepatic SREBP1 signals increased from 2nd to 6th week, but decreased at 8th week due to substantiated insulin resistance (plasma insulin levels, plasma glucose levels, and P-AKTSer473 levels) in HCD group. Importantly, the hepatic carbohydrate response element binding protein (ChREBP) signals (positive hepatocytes, fluorescence intensity, and expression levels) were all significantly elevated by HCD-induced glucose-6-phosphate (G6P) accumulation at 2nd, 4th, 6th, and 8th week (P < 0.05). Compared to 2nd and 4th week, the hepatic ChREBP signals and G6P contents was significantly increased by HCD at 6th and 8th week (P < 0.05). The HCD-induced G6P accumulation was caused by the significantly increased expression of hepatic gck, pklr, and glut2 (P < 0.05) but not 6pfk at 4th, 6th, and 8th week, compared to NCD group. These results suggested that the HCD-induced hepatic lipid deposition was mainly promoted by SREBP1 in earlier stage and by ChREBP in later stage for gibel carp. This study revealed the sequential regulation pathways of the conversion from feed carbohydrate to body lipid in fish.

Decreased cardiovascular risk factors and inflammation with remission of type 2 diabetes in adults with obesity using a high protein diet: Randomized control trial

ObjectiveThe study objective was to determine the effects a high protein (HP) vs. a high carbohydrate (HC) diet on cardiovascular risk factors (CVR), inflammation, metabolic parameters, oxidative stress, weight loss, lean and fat body mass, and remission of Type 2 Diabetes (T2DM) in subjects with obesity. Research design and methodsTwelve women and men with T2D were recruited and randomized to either a HP (30%protein, 30%fat, 40%carbohydrate) (n = 6) or HC (15%protein, 30%fat, 55%carbohydrate) (n = 6) diet feeding study for 6 months in this randomized controlled trial. All meals were purchased at local grocery stores and provided to subjects for 6 months with daily food menus for HP or HC compliance with weekly food pick-up and weight measurements. Oral glucose tolerance and meal tolerance tests with glucose and insulin measurements and DXA scans were done at baseline and after 6 months on the respective diets. ResultsAfter 6 months on the HP diet, 100% of the subjects had remission of their T2DM to Normal Glucose Tolerance (NGT), whereas only 16.6% of subjects on the HC diet had remission of their T2DM. The HP diet group exhibited significant improvement in a) cardiovascular risk factors (p = 0.004, b) inflammatory cytokines(p = 0.001), c) insulin sensitivity(p = 0.001), d) oxidative stress(p = 0.001), e) increased %lean body mass(p = 0.001) compared to the HC diet group at 6 months. ConclusionsA significant improvement in cardiovascular risk factors, inflammation, metabolic parameters and 100% remission of T2DM to NGT was achieved with a HP diet compared to a HC diet at 6 months. Clinicaltrials.gov. identifierNCT01642849.

Insufficient or excessive dietary carbohydrates affect gut health through change in gut microbiota and regulation of gene expression of gut epithelial cells in grass carp (Ctenopharyngodon idella)

Dietary carbohydrate levels can affect gut health, but the roles played by gut microbiota and gut epithelial cells, and their interactions remain unclear. In this experiment, we investigated gut health, gut microbiota, and the gene expression profiles of gut epithelial cells in grass carp consuming diets with different carbohydrate levels. Compared to the moderate-carbohydrate diet, low-carbohydrate diet significantly increased the relative abundance of pathogenic bacteria (Ralstonia and Elizabethkingia) and decreased the abundance of metabolism in cofactors and vitamins, implying a dysregulated gut microbiota and compromised metabolic function. Moreover, low-carbohydrate diet inhibited the expression levels of key genes in autophagy-related pathways in gut epithelial cells, which might directly lead to reduced clearance of defective organelles and pathogenic microorganisms. These aforementioned factors may be responsible for the imperfect organization of the intestinal tract. High-carbohydrate diet also significantly increased the abundance of pathogenic bacteria (Flavobacterium), which directly contributed to a decrease in the abundance of immune system of the microbiota. Furthermore, the active pathways of staphylococcus aureus infection and complement and coagulation cascades, as well as the inhibition of the glutathione metabolism pathway were observed. Above results implied that high-carbohydrate diet might ultimately cause severe gut damage by affecting immune function of microbiota, mentioned immune-related pathways, and the antioxidant capacity. Finally, the correlation network diagram revealed strong correlations of the differentially immune-related gene major histocompatibility complex class I antigen (MR1) with Enhydrobacter and Ruminococcus_gnavus_group in low-carbohydrate diet group, and Arenimonas in high-carbohydrate diet group, respectively, suggesting that MR1 might be a central target for immune responses in gut epithelial cells induced by gut microbiota at different levels of dietary carbohydrate. All these results provided insight in the development of antagonistic probiotics and target genes to improve the utilization of carbohydrate.

Effect of dietary carbohydrate on glycometabolism of juvenile golden pompano (Trachinotus ovatus) related to growth performance, hepatic histopathology, transcriptome profiles and identification of differentially expressed genes

A hepatic transcriptome was produced through the technology of RNA sequencing and short-read assembly in golden pompano Trachinotus ovatus fed with three experimental diets respectively containing low carbohydrate diet (LCD), intermediate carbohydrate diet (MCD), and high carbohydrate diet (HCD). In total, 57,217 unigenes were acquired in the current study, with average length 1182.24 bp. 21,920, 22,514 and 24,680 unigenes were acquired from LCD, MCD and HCD groups, respectively. There were 1513 differential expressed genes in LCD and MCD groups, with 676 up- and 837 down-regulated genes in LCD group; 2369 genes were differentially expressed between HCD vs MCD, containing 1397 up and 972 down-regulated genes in HCD group. 1686 differential expressed genes were observed in the comparison of HCD and LCD, containing 1044 up- and 642 down-regulated genes in HCD group. Some differential expressed genes, such as hexokinase-1-like isoform X3, pancreatic alpha-amylase-like, hexokinase-1-like isoform X1, ADP-dependent glucokinase isoform X2, fructose-bisphosphate aldolase A-like, and acetyl-CoA carboxylase isoform X8, were related to carbohydrate metabolism, indicating these genes in the golden pompano were in response to dietary carbohydrate. In this study, long-chain-fatty-acid-CoA ligase 5 was up-regulated in comparison of HCD_vs_MCD and HCD_vs_LCD, which indicated that FACL5 may be sensitive to high dietary carbohydrate. This result coincides with the pathological changes of hepatocyte morphology in the present study. The results of transcriptome analysis in this study were confirmed by RT-PCR in 14 randomly selected unigenes. This study may provide novel data and theoretical support on hepatic transcriptome information of the golden pompano, which is a vital resource for studies of bioinformatics in golden pompano. Besides, the present study identifies some pivotal genes related to dietary carbohydrate and lipid deposition, which will accumulate data on carbohydrate and/or lipid metabolism in marine fish species to support related research.

Characterizing the Effects of High Fat and High Carbohydrate Diets on Feeding Behavior and Energy Expenditure in Mice

ObjectiveWe sought to characterize how different compositions of the diet can alter feeding behavior and energy expenditure in mice, ultimately driven by changes in sympathetic activation and thermogenesis.HypothesisMice on a high fat diet (HFD) will consume more calories/day compared to high carbohydrate diet (HCD) and standard chow fed mice. Mice on HFD will have decreased expression of UCP1 in both brown and white adipose tissue. There will be decreased expression for several lipolytic enzymes in the white adipose of HFD mice.MethodsA total of 21 mice were divided into three ad libitum fed diet groups: HFD, HCD, and standard chow. Each group was fed their respective diet for 7 weeks. Changes in weight and percent body fat were recorded by NMR. At week 5, glucose tolerance tests were performed on all mice. Both a 24‐hour heat production and respiratory exchange ratio were collected on each group using a metabolic cage system. Mice were sacrificed at the conclusion of week 7 and organs were collected for molecular analysis.ResultsWe show that mice on both ad libitum HFD and HCD consume significantly more calories/day when compared to standard chow. Both HFD and HCD fed mice have a significantly increased body weight and percent body fat when compared to standard chow; however, the HFD mice had a far greater increase in weight compared to HCD fed mice despite no difference in calorie consumption. Mice on a HFD had a lower 24‐hour average heat production per body mass when compared to standard chow and HCD mice and a significantly impaired glucose tolerance test. Furthermore, UCP1 mRNA expression is significantly elevated in brown adipose tissue (BAT) of HCD mice compared to that of HFD and standard chow mice. There were no differences in UCP1 expression in subcutaneous or visceral white adipose tissue (WAT) among all groups. There were also no differences in tyrosine hydroxylase (TH) expression in BAT between all mice. Three markers of lipolysis were decreased in visceral WAT of HFD mice compared to HCD and standard chow counterparts.DiscussionMice consumed significantly more calories when fed a HFD or HCD. These mice gain significantly more weight compared to chow with HFD mice gaining weight far more than the HCD group. This major difference in weight gain despite no significant difference in calorie consumption between HFD and HCD suggests differences may be determined by energy expenditure. This evidence is further supported by the fact that HFD fed mice had a significantly lower daily heat production compared to HCD and standard chow mice. We also show that HCD increases thermogenesis in mouse BAT which may be protective against weight gain. Finally, lipolysis signaling seems to be impaired in HFD mice, but no data supports that this is due to differences in sympathetic activation. Further work will include analyzing the same tissues in isocaloric, restricted diet fed mice.

Preoperative Short-term High-Carbohydrate Diet Provides More High-Quality Transplantable Fat and Improves the Outcome of Fat Grafts in Mice.

Patients with a low BMI may have inadequate high-quality adipose tissue for transplantation. The influence of high-energy diets on adipose tissue and graft retention remains unknown. The authors explored inguinal fat pad alternation in mice fed on a short-time high-fat diet (HFD) or a high-carbohydrate diet (HCD) preoperatively and the morphological and histological differences after transplantation. Mice were fed HFD (60% kcal from fat, 20% from carbohydrate), HCD (9.3% kcal from fat, 80.1% from carbohydrate), or normal (12% kcal from fat, 67% kcal from carbohydrate) diets for 2 or 4 weeks. Histological analyses were carried out following hematoxylin and eosin staining as well as CD34 and proliferating cell nuclear antigen immunostaining. The uncoupling protein-1 expression was determined by western blotting. Fat pads from each group were grafted into the dorsal region of the recipient mice, and morphological and histological changes were determined 4, 8, and 12 weeks posttransplantation. Vascular endothelial growth factor-α and platelet-derived growth factor-α expression were determined using quantitative polymerase chain reaction. The inguinal fat pad volume increased in the HFD and HCD groups. The presence of multilocular adipocytes in inguinal fat of HCD-fed mice, combined with the increased uncoupling protein-1 content, suggested adipocyte browning. HCD grafts showed higher volume retention and reduced oil cyst formation, possibly attributed to better angiogenesis and adipogenesis. HCD enlarged adipose tissue and improved graft survival rates, which may be due to the browning of fat before grafting and enhanced angiogenesis after grafting.

High-carbohydrate diet altered conversion of metabolites, and deteriorated health in juvenile largemouth bass

To explore the effects of dietary carbohydrate level on nutrients metabolism, largemouth bass juveniles (initial weight, 4.0 ± 0.2 g) were fed three isonitrogenous and isoenergetic diets containing 9.66% (L), 14.32% (M) or 19.11% (H) carbohydrate for 8 weeks. The lowest weight gain (15.75 ± 0.76 g) was observed in group H. Feeding high carbohydrate diet (HCD) led to increased pyruvate (PA), lactic acid (LD), triglyceride (TG) and free fatty acids (NEFA) levels in plasma. Also, HCD enhanced vacuolation, glycogen granule and lipid accumulation in fish liver. Activities of hepatic glycolysis enzymes such as hexokinase, pyruvate kinase and lactate dehydrogenase did not significantly differ among treatments ( P > 0.05). HCD resulted in enhancement of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and lipase (LPS) activities, and increased glycogen and triglyceride (TG) concentrations. Similarly, expression of glucose and lipid metabolism related genes such as glycogen phosphorylase (PYG) and carnitine palmitoyl transferases (CPT1, CPT2) were up-regulated with increasing carbohydrate level. Hepatic catalase (CAT) and glutathione peroxidase (GSH-PX) activities, and total antioxidant capacity (T-AOC) were decreased in HCD group. UPLC-MS metabolomics revealed that glucose metabolism, lipid metabolism, and antioxidant defense system were influenced by dietary carbohydrate level. HCD raised the accumulation of carbohydrate metabolites (phosphohydroxypyruvic acid), unsaturated fatty acids (19( R )-HETE, 9( S )-HPOT, alpha-Linolenic acid and oleic acid), cholesterol, and antioxidant functional substance (oxidized glutathione). Additionally, these differential metabolites were enriched in the metabolic pathways such as galactose metabolism, fructose and mannose metabolism, unsaturated fatty acid biosynthesis, primary bile acid biosynthesis, cholesterol-butyrate metabolism, glutathione metabolism, serine and threonine metabolism. Overall, our results revealed the details of metabolites conversion in juvenile largemouth bass fed HCD. • High-carbohydrate diet (HCD) led to the accumulation of glycogen, lipid droplets and occurrence of vacuolation in liver. • HCD induced antioxidant response through the glutathione antioxidant system. • HCD promoted the conversion of glucose to other carbohydrates, lipids and protein components.

Apple Polyphenols Extracts Ameliorate High Carbohydrate Diet-Induced Body Weight Gain by Regulating the Gut Microbiota and Appetite.

To investigate the potential contribution of appetite regulation and modulation of gut microbiota to the ameliorated effects of apple polyphenols extracts (APE) on high carbohydrate diet (HCD)-induced body weight (BW) gain, we conducted this study. One hundred C57BL/6 male mice were randomly divided into seven groups and fed with the following diets for 12 weeks: chow diet (CON), HCD (HCD), high fructose and sucrose diet (HSCD), and HCD and HSCD with 125 or 500 mg/kg·day APE gavage. Compared to the CON group, the BW of mice in the HCD and HSCD groups increased significantly. HSCD induced a more significant weight gain in the white adipose tissue (WAT) and liver than HCD, accompanied by severe impairment of glucose tolerance and a larger diameter of adipocytes. On the other hand, by decreasing food intake, APE significantly reduced BW via mechanisms, including decreased weights of the WAT and liver, amelioration of glucose tolerance, and amplification of WAT browning by upregulating the mRNA levels of Ucp-1 and Cidea. Moreover, APE promoted transcription and secretion of GLP-1, with the increased expression of gut anorexigenic hormone peptides Ffar 2/3 in the colon and anorectic neuropeptide gene expression of Pomc, Cart, and Mc4r in the hypothalamus, causing increased satiety. Additionally, APE significantly increased Verrucomicrobia colonization and the relative abundance of Akkermansia. APE potentially ameliorates high simple carbohydrate diet-induced body weight gain by mechanisms related to gut microbiota regulation and appetite inhibition.

Prefrontal Cortex and Hippocampus Inflammation in Mice Fed High-Carbohydrate or High-Fat Diets.

We previously reported that a high-carbohydrate diet (HCD) induced systemic inflammation and higher gene expression of proinflammatory mediators in the liver, skeletal muscle, and brain than a high-fat diet (HFD). However, the differences between the groups were less pronounced in the brain. In this study, we extended the evaluation of inflammation to specific areas of the brain. In this study, we evaluated the gene expression of caspase 2, caspase 3, caspase 9, cyclooxygenase-2 (Cox 2), inducible nitric oxide synthase (iNOS), interleukin (IL), IL-6, IL-1β, IL-10, IL-4, tumor necrosis factor-alpha (TNF-α), integrin subunit alpha m (Itgam), S100 protein (S100), allograft inflammatory factor 1 (Aif1), and glial fibrillary acidic protein (Gfap) in the prefrontal cortex and hippocampus of male Swiss mice that were fed with HCD or HFD for 8 weeks. The HCD group exhibited higher IL-1β expression, whereas the HFD group showed higher TNF-α expression in the prefrontal cortex. In the hippocampus, TNF-α expression was higher in the HFD group. IL-1β and TNF-α are proinflammatory cytokines that have been associated with impaired brain function and numerous brain disorders. Our results indicate that both HCD and HFD promote prefrontal cortex inflammation; however, the hippocampus seems more sensitive to a HFD than HCD.

Bacillus amyloliquefaciens ameliorates high-carbohydrate diet-induced metabolic phenotypes by restoration of intestinal acetate-producing bacteria in Nile Tilapia.

Poor utilisation efficiency of carbohydrate always leads to metabolic phenotypes in fish. The intestinal microbiota plays an important role in carbohydrate degradation. Whether the intestinal bacteria could alleviate high-carbohydrate diet (HCD)-induced metabolic phenotypes in fish remains unknown. Here, a strain affiliated to Bacillus amyloliquefaciens was isolated from the intestine of Nile tilapia. A basal diet (CON), HCD or HCD supplemented with B. amy SS1 (HCB) was used to feed fish for 10 weeks. The beneficial effects of B. amy SS1 on weight gain and protein accumulation were observed. Fasting glucose and lipid deposition were decreased in the HCB group compared with the HCD group. High-throughput sequencing showed that the abundance of acetate-producing bacteria was increased in the HCB group relative to the HCD group. Gas chromatographic analysis indicated that the concentration of intestinal acetate was increased dramatically in the HCB group compared with that in the HCD group. Glucagon-like peptide-1 was also increased in the intestine and serum of the HCB group. Thus, fish were fed with HCD, HCD supplemented with sodium acetate at 900 mg/kg (HLA), 1800 mg/kg (HMA) or 3600 mg/kg (HHA) diet for 8 weeks, and the HMA and HHA groups mirrored the effects of B. amy SS1. This study revealed that B. amy SS1 could alleviate the metabolic phenotypes caused by HCD by enriching acetate-producing bacteria in fish intestines. Regulating the intestinal microbiota and their metabolites might represent a powerful strategy for fish nutrition modulation and health maintenance in future.

PM2.5 induces intestinal damage by affecting gut microbiota and metabolites of rats fed a high-carbohydrate diet.

PM2.5 has a major impact on the gastrointestinal system, but the specific mechanism behind this action is not fully understood. Current studies have focused on the relationship between PM2.5 and intestinal flora disorder, while ignoring the important influence of diet on gut microbes. In this study, SD rats were fed either a normal, high-fat, or high-carbohydrate diet for two months and exposed to PM2.5 (7mg/kg b.w.) by intratracheal instillation. The results showed that the body and kidney weights of the rats in the high-fat diet group were significantly increased relative to those with a normal diet, and changes in the intestinal microbes and metabolites induced by PM2.5 were observed. Rats in the high-carbohydrate diet group had a significant response, and the diversity and richness indices of the flora were reduced (p<0.05); additionally, intestinal Biffidobacterium and Lactobacillus were enriched, while many endogenous metabolites were found. Some amino acids derivatives and long-chain fatty acids were increased (p<0.05). Both diet structure and PM2.5 exposure can affect the composition of gut microbiota, and intestinal metabolites may be associated with cell membrane damage when a high-carbohydrate diet interacts with PM2.5. This study considers multiple dietary factors to further supplement the evidence of intestinal damage via PM2.5.

A mouse model of short-term, diet-induced fatty liver with abnormal cardiolipin remodeling via downregulated Tafazzin gene expression.

Cardiolipin (CL) helps maintain mitochondrial structure and function. Here we investigated whether a high carbohydrate diet (HCD) fed to mice for a short period (5 days) could modulate the CL level, including that of monolysoCL (MLCL) in the liver. Total CL in the HCD group was 22% lower than that in the normal chow diet (NCD) group (P < 0.05). The CL72:8 level strikingly decreased by 93% (P < 0.0001), whereas total nascent CLs (CLs other than CL72:8) increased (P < 0.01) in the HCD group. The total MLCL in the HCD group increased by 2.4-fold compared with that in the NCD group (P < 0.05). Tafazzin expression in the HCD group was significantly downregulated compared with that in the NCD group (P < 0.05). A strong positive correlation between nascent CL and total MLCL (r=0.955, P < 0.0001), and a negative correlation between MLCL and Tafazzin expression (r=-0.593, P=0.0883) were observed. A HCD modulated the fatty acid composition of CL and MLCL via Tafazzin in the liver, which could lead to mitochondrial dysfunction. This model may be useful for elucidating the relationship between fatty liver and mitochondrial dysfunction. © 2021 Society of Chemical Industry.

Hyperinsulinemia Induced Altered Insulin Signaling Pathway in Muscle of High Fat- and Carbohydrate-Fed Rats: Effect of Exercise.

Insulin resistance is a state of impaired responsiveness to insulin action. This condition not only results in deficient glucose uptake but increases the risk for cardiovascular diseases (CVD), stroke, and obesity. The present work investigates the molecular mechanisms of high carbohydrate and fat diet in inducing prediabetic hyperinsulinemia and effect of exercise on InsR signaling events, muscular AChE, and lactate dehydrogenase activity. Adult male Wistar rats were divided into the control (C) diet group, high-carbohydrate diet (HCD) group, high-fat diet (HFD) group, and HCD and HFD groups with exercise (HCD Ex and HFD Ex, respectively). Acetyl choline esterase activity, lactate dehydrogenase activity, total lactate levels, IRS1 phosphorylations, and Glut4 expression patterns were studied in the muscle tissue among these groups. High carbohydrate and fat feeding led to hyperinsulinemic status with reduced acetylcholine esterase (AChE) activity and impaired phosphorylation of IRS1 along with increased lactate concentrations in the muscle. Exercise significantly upregulated phosphoinositide 3 kinase (PI3K) docking site phosphorylation and downregulated the negative IRS1 phosphorylations thereby increasing the glucose transporter (GLUT) expressions and reducing the lactate accumulation. Also, the levels of second messengers like IP3 and cAMP were increased with exercise. Increased second messenger levels induce calcium release thereby activating the downstream pathway promoting the translocation of GLUT4 to the plasma membrane. Our results showed that the metabolic and signaling pathway dysregulations seen during diet-induced hyperinsulinemia, a metabolic condition seen during the early stages in the development of prediabetes, were improved with vigorous physical exercise. Thus, exercise can be considered as an excellent management approach over drug therapy for diabetes and its complications.

Gemfibrozil improves lipid metabolism in Nile tilapia Oreochromis niloticus fed a high-carbohydrate diet through peroxisome proliferator activated receptor-α activation

High carbohydrate diet (HCD) can induce lipid metabolism disorder, characterized by excessive lipid in farmed fish. Peroxisome proliferator activated receptor-α (PPARα) plays an important role in lipid homeostasis. In this study, we hypothesize that PPARα can improve lipid metabolism in fish fed HCD. Fish (3.03 ± 0.11 g) were fed with three diets: control (30% carbohydrate), HCD (45% carbohydrate) and HCG (HCD supplemented with 200 mg/kg gemfibrozil, an agonist of PPARα) for eight weeks. The fish fed HCG had higher growth rate and protein effiency than those fed the HCD diet, whereas the opposite trend was observed in feed conversion ratio, hepatosomatic index and mesenteric fat index. Additionally, fish fed HCG significantly decreased lipid accumulation in the whole body, liver and adipose tissues compared to those fed the HCD diet. Furthermore, fish in the HCG group significantly increased the mRNA and protein expression and protein dephosphorylation of PPARα. The HCG group also significantly increased the mRNA level of the downstream target genes of PPARα, whereas the opposite trend occured in the mRNA level of lipolysis-related genes compared to the HCD group. Besides, fish in the HCG group remarkably decreased the contents of alanine aminotransferase, aspartate aminotransferase and malondialdehyde, whereas the opposite occured in the activities of antioxidative enzymes and anti-inflammatory cytokine genes compared to the HCD group. This study indicates that gemfibrozil can improve lipid metabolism and maintain high antioxidant and anti-inflammatory capacity through activating PPARα in Nile tilapia fed a high carbohydrate diet.

Effect of High Carbohydrate Diet on Complete Freund’s Adjuvant Induced Inflammation in Rats

Chronic low grade inflammation is an essential pathological feature of a variety of non-communicable diseases (NCDs). These diseases have now superseded infectious diseases where the burden of disease is concerned. One of the important modifiable factors contributing to chronic disease is food high in carbohydrate. This study was planned to study the role of high carbohydrate diet on a model of inflammation induced by Complete Freund’s adjuvant (CFA) in male Wistar rats. Animals were divided into 3 groups of 10 rats each. Group I fed with standard diet serving as control; Group II fed with high carbohydrate diet (HCD) and Group III fed with standard diet serving as disease free normal group. CFA was injected subcutaneously into the hind paw 4weeks after starting the diet into groups I and II only. Diet was continued for up to 21days after CFA injection. Digital plethysmometer measured the paw volume. Blood obtained before euthanasia served for estimating cytokines and oxidative stress parameters. A rise in paw edema was seen in control and high carbohydrate diet groups up to day 21. In the high carbohydrate group there were high serum cytokine levels and significant depletion of antioxidant enzymes. The authors conclude that, a high carbohydrate diet contributes significantly to the process of inflammation which has now been established as a significant factor in the causation of NCDs. Therefore it would be prudent to restrict carbohydrates in our diet.

Multigenerational effects of dietary macronutrient intake on the metabolic phenotype of male Wistar rats.

Gene-nutrient interactions are implicated in metabolic phenotypes like metabolic syndrome. The aim of this study was to examine the effects of diet-induced metabolic phenotypes in rats and investigate the effects of these phenotypes in three successive generations. Three generations of rats were fed on different diets and mated. Blood glucose, adiposity, lipid profile, insulin, adipocytokines, ghrelin, and corticosterone concentrations were determined in F0, F1, and F2 generations using standard methods. In comparison with control across generations, glucose (32%), triacylglycerols (52%), and insulin (10%) were significantly elevated in the high-fat diet (HFD)-fed rats; total cholesterol was higher in HFD and high-carbohydrate diet (HCD)-fed groups; whereas high density lipoprotein was higher in the HFD rats but lower in the HPD rats. Adipocytokines were significantly higher in the HCD and HFD groups but lower in the high-protein diet group, whereas ghrelin only declined in HFD rats. This study revealed that different dietary macronutrients induced distinctive metabolic phenotypes, which had variable effects in different generations.

Dietary salmon milt extracts attenuate hepatosteatosis and liver dysfunction in diet-induced fatty liver model.

Dietary nucleotides have several reported beneficial effects. Here, we report on a proteomic analysis of the effect of dietary nucleotides-rich salmon milt extract (SME) on the liver in a diet-induced fatty liver model. Young male normal ddY mice were fed a normal chow diet, high carbohydrate diet (HCD), HCD containing 1% SME, or HCD containing 10% SME for 5 days following by a 2-day fast. Increased serum alanine transferase and aspartate transferase activities were observed in the HCD group and were significantly attenuated in the SME groups (P < 0.05). Hepatic steatosis was observed in all the HCD groups. Hepatic expression of Tnfα was significantly suppressed in the 10% SME group (P < 0.05). Comprehensive proteomic analysis of the liver in the SME groups revealed an increase in the levels of major proteins involved in mitochondrial bioenergetics, including peroxisome proliferator-activated receptor gamma co-activator 1 alpha, mitochondrial thioredoxin, cardiolipin synthase, peroxisome proliferator-activated receptor alpha, and carnitine palmitoyltransferase I. Dietary SME improved liver function in the diet-induced fatty liver model. Activation of mitochondrial biogenetic function might be involved in this process. © 2018 Society of Chemical Industry.

Brain Fatty Acid Composition and Inflammation in Mice Fed with High-Carbohydrate Diet or High-Fat Diet.

Both high fat diet (HFD) and high carbohydrate diet (HCD) modulate brain fatty acids (FA) composition. Notwithstanding, there is a lack of information on time sequence of brain FA deposition either for HFD or HCD. The changes in brain FA composition in mice fed with HFD or HCD for 7, 14, 28, or 56 days were compared with results of 0 (before starting given the diets). mRNA expressions of allograft inflammatory factor 1 (Aif1), cyclooxygenase-2 (Cox 2), F4/80, inducible nitric oxide synthase (iNOS), integrin subunit alpha m (Itgam), interleukin IL-1β (IL-1β), IL-6, IL-10, and tumor necrosis factor alpha (TNF-α) were measured. The HFD group had higher speed of deposition of saturated FA (SFA), monounsaturated FA (MUFA), and polyunsaturated FA (PUFA) at the beginning of the experimental period. However, on day 56, the total amount of SFA, MUFA, and PUFA were similar. mRNA expressions of F4/80 and Itgam, markers of microglia infiltration, were increased (p < 0.05) in the brain of the HCD group whereas inflammatory marker index (IMI) was higher (46%) in HFD group. In conclusion, the proportion of fat and carbohydrates in the diet modulates the speed deposition of FA and expression of inflammatory gene markers.