Refined Carbohydrate Diet Research Articles

Plasma Metabolite Response to Simple, Refined and Unrefined Carbohydrate-Enriched Diets in Older Adults—Randomized Controlled Crossover Trial

Food intake data collected using subjective tools are prone to inaccuracies and biases. An objective assessment of food intake, such as metabolomic profiling, may offer a more accurate method if unique metabolites can be identified. To explore this option, we used samples generated from a randomized and controlled cross-over trial during which participants (N = 10; 65 ± 8 year, BMI, 29.8 ± 3.2 kg/m2) consumed each of the three diets enriched in different types of carbohydrate. Plasma metabolite concentrations were measured at the end of each diet phase using gas chromatography/time-of-flight mass spectrometry and ultra-high pressure liquid chromatography/quadrupole time-of-flight tandem mass spectrometry. Participants were provided, in random order, with diets enriched in three carbohydrate types (simple carbohydrate (SC), refined carbohydrate (RC) and unrefined carbohydrate (URC)) for 4.5 weeks per phase and separated by two-week washout periods. Data were analyzed using partial least square-discrimination analysis, receiver operating characteristics (ROC curve) and hierarchical analysis. Among the known metabolites, 3-methylhistidine, phenylethylamine, cysteine, betaine and pipecolic acid were identified as biomarkers in the URC diet compared to the RC diet, and the later three metabolites were differentiated and compared to SC diet. Hierarchical analysis indicated that the plasma metabolites at the end of each diet phase were more strongly clustered by the participant than the carbohydrate type. Hence, although differences in plasma metabolite concentrations were observed after participants consumed diets differing in carbohydrate type, individual variation was a stronger predictor of plasma metabolite concentrations than dietary carbohydrate type. These findings limited the potential of metabolic profiling to address this variable.

Beta-Cryptoxanthin Supplementation Protects Against Liver Cancer Progression and Correlates With Altered Targeted and Untargeted Metabolomic Profiles in Mice

ObjectivesNonalcoholic fatty liver disease (NAFLD)-associated hepatocellular carcinoma (HCC) is expected to increase globally in the upcoming years. Diets high in refined carbohydrates and added sugars (HRCD) have been linked to NAFLD progression. Previous studies have demonstrated that retinoids possess anti-tumorigenic properties, yet less is known about whether upstream provitamin A carotenoids exhibit similar characteristics. We recently demonstrated that dietary beta-cryptoxanthin (BCX), a provitamin A carotenoid, decreased NAFLD severity and HCC progression in diethylnitrosamine (DEN)-initiated, high refined carbohydrate diet (HRCD)-fed mice. In this study, we evaluated the effects of dietary BCX supplementation on modulating plasma biomarkers, hepatic vitamin A status, and plasma metabolomic profiles in our DEN-initiated, HRCD-promoted model of HCC. MethodsMale, six-week-old C57BL/6J mice were injected with DEN (25 mg/kg BW) and a fed a HRCD (66.5% carbs including sucrose) with or without BCX supplementation (10 mg/kg diet) for 24 weeks. Using plasma samples, we performed metabolomics using our UHPLC-QTOF-MS platform, a targeted Biocrates MxP Quant 500 kit, and a complimentary untargeted analysis of phospholipids from the METLIN database to identify metabolites which correlate with primary outcomes. Hepatic vitamin A levels were determined via HPLC. ResultsCompared to HRCD-fed, DEN-injected mice, mice fed BCX displayed significantly lower tumor burden and steatosis, higher hepatic vitamin A status, and lower plasma levels of alanine transaminase (ALT) and lactate dehydrogenase (LDH). Moderate negative correlations were also identified amongst hepatic vitamin A levels and primary outcomes, such as HCC tumor number, steatosis score, and relevant biomarkers. Our metabolomics data showed significant modulations in metabolites with BCX treatment from phosphatidylcholine, sphingomyelin, ceramide, bile acid, and other phospholipid classes. ConclusionsBCX supplementation significantly reduced HCC severity, increased hepatic vitamin A status, reduced plasma levels of ALT and LDH, and altered several lipid-related classes of metabolites, thus supporting a chemopreventive potential for BCX against HRCD-promoted HCC development. Funding SourcesUSDA/ARS and NIFA/AFRI.

Ablation of Carotenoid Cleavage Enzymes BCO1 & BCO2 Alters Gut Microbial and Plasma Metabolomic Profiles in High Refined Carbohydrate Diet-Fed Mice

Objectivesβ-Carotene-15,15′-oxygenase (BCO1) and β-carotene-9′,10′-oxygenase (BCO2) cleave carotenoids to form vitamin A or apo-carotenoid species. Beyond these roles, BCO1 and BCO2 have been implicated in modulating lipid, cholesterol, and oxidative stress-related processes, yet less is known about their combined influence on shaping gut microbial and plasma metabolic profiles. Current intake of refined carbohydrates and added sugars exceeds the recommendations within the Dietary Guidelines for Americans, which may contribute to the development of nonalcoholic fatty liver disease (NAFLD). In the present study, we aimed to uncover whether mice with systemic ablation of BCO1-/-/BCO2-/- (DKO) display distinctive phenotypes in response to a high refined carbohydrate diet (HRCD) model of NAFLD. MethodsMale, six-week-old C57BL/6J wild type mice (WT) and DKO mice were fed a chow diet or a HRCD (66.5% carbs including sucrose) for 24 weeks. We used fecal and plasma samples to respectively perform 16S rDNA sequencing, and both targeted and untargeted metabolomics using our UHPLC-QTOF-MS platform, a targeted Biocrates MxP Quant 500 kit, and a complimentary untargeted analysis of phospholipids from the METLIN database. Data were analyzed using QIIME2-DEseq2, MetaboAnalyst 5.0, MassHunter Qualitative Analysis, and MicrobiomeAnalyst. ResultsHRCD-fed WT and DKO mice developed similar levels of hepatic steatosis although DKO mice had significantly higher hepatic levels of malondialdehyde (MDA). Interestingly, in both chow-fed and HRCD-fed DKO mice, plasma adiponectin and hepatic bile acids were significantly lower compared to respective WT groups. Our metabolomics data revealed that DKO mice displayed significant alterations in ceramide, cholesterol ester, triglyceride, and phospholipid classes under both chow and HRCD conditions. Additionally, when compared to HRCD-fed WT mice, HRCD-fed DKO mice displayed significantly reduced alpha diversity and possessed significant compositional differences based on Bray Curtis dissimilarity measures. ConclusionsBCO1/BCO2 DKO mice display altered metabolomic and gut microbial profiles. Carotenoid cleavage enzymes affect diverse physiological processes, which involve lipid metabolism and the gut microbiome. Funding SourcesUSDA/ARS and NIFA/AFRI.

Exploring changes in the human gut microbiota and microbial-derived metabolites in response to diets enriched in simple, refined, or unrefined carbohydrate-containing foods: a post hoc analysis of a randomized clinical trial

Dietary carbohydrate type may influence cardiometabolic risk through alterations in the gut microbiome and microbial-derived metabolites, but evidence is limited. We explored the relative effects of an isocaloric exchange of dietary simple, refined, and unrefined carbohydrate on gut microbiota composition/function, and selected microbial metabolite concentrations. Participants [n=11; age: 65±8 y; BMI (in kg/m2): 29.8±3.2] were provided with each of 3 diets for 4.5 wk with 2-wk washout, according to a randomized, crossover design. Diets [60% of energy (%E) carbohydrate, 15%E protein, and 25%E fat] differed in type of carbohydrate. Fecal microbial composition, metatranscriptomics, and microbial-derived SCFA and secondary bile acid (SBA) concentrations were assessed at the end of each phase and associated with cardiometabolic risk factors (CMRFs). Roseburia abundance was higher (11% compared with 5%) and fecal SBA concentrations were lower (lithocolic acid -50% and deoxycholic acid -64%) after consumption of the unrefined carbohydrate diet relative to the simple carbohydrate diet [false discovery rate (FDR): all P<0.05), whereas Anaerostipes abundance was higher (0.35% compared with 0.12%; FDR: P=0.04) after the simple carbohydrate diet relative to the refined carbohydrate diet. Metatranscriptomics indicated upregulation of 2 cellular stress genes (FDR: P<0.1) after the unrefined carbohydrate diet compared with the simple carbohydrate or refined carbohydrate diets. The microbial expression of 3 cellular/oxidative stress and immune response genes was higher (FDR: P<0.1) after the simple carbohydrate diet relative to the refined carbohydrate diet. No significant diet effect was observed in fecal SCFA concentrations. Independent of diet, we observed 16 associations (all FDR: P<0.1) of taxon abundance (15 phylum and 1 genera) with serum inflammatory markers and also with fecal SCFA and SBA concentrations. Consuming an unrefined carbohydrate-rich diet had a modest effect on the gut microbiome and SBAs, resulting in favorable associations with selected CMRFs. Simple carbohydrate- and refined carbohydrate-rich diets have distinctive effects on the gut microbiome, suggesting differential mechanisms mediate their effects on cardiometabolic health. This trial was registered at clinicaltrials.gov as NCT01610661.

Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management.

Risk factors for COVID-19 patients with poorer outcomes include pre-existing conditions: obesity, type 2 diabetes mellitus, cardiovascular disease (CVD), heart failure, hypertension, low oxygen saturation capacity, cancer, elevated: ferritin, C reactive protein (CRP) and D-dimer. A common denominator, hyperinsulinaemia, provides a plausible mechanism of action, underlying CVD, hypertension and strokes, all conditions typified with thrombi. The underlying science provides a theoretical management algorithm for the frontline practitioners.Vitamin D activation requires magnesium. Hyperinsulinaemia promotes: magnesium depletion via increased renal excretion, reduced intracellular levels, lowers vitamin D status via sequestration into adipocytes and hydroxylation activation inhibition. Hyperinsulinaemia mediates thrombi development via: fibrinolysis inhibition, anticoagulation production dysregulation, increasing reactive oxygen species, decreased antioxidant capacity via nicotinamide adenine dinucleotide depletion, haem oxidation and catabolism, producing carbon monoxide, increasing deep vein thrombosis risk and pulmonary emboli. Increased haem-synthesis demand upregulates carbon dioxide production, decreasing oxygen saturation capacity. Hyperinsulinaemia decreases cholesterol sulfurylation to cholesterol sulfate, as low vitamin D regulation due to magnesium depletion and/or vitamin D sequestration and/or diminished activation capacity decreases sulfotransferase enzyme SULT2B1b activity, consequently decreasing plasma membrane negative charge between red blood cells, platelets and endothelial cells, thus increasing agglutination and thrombosis.Patients with COVID-19 admitted with hyperglycaemia and/or hyperinsulinaemia should be placed on a restricted refined carbohydrate diet, with limited use of intravenous dextrose solutions. Degree/level of restriction is determined by serial testing of blood glucose, insulin and ketones. Supplemental magnesium, vitamin D and zinc should be administered. By implementing refined carbohydrate restriction, three primary risk factors, hyperinsulinaemia, hyperglycaemia and hypertension, that increase inflammation, coagulation and thrombosis risk are rapidly managed.

A four-week white bread diet does not alter plasma glucose concentrations, metabolic or vascular physiology in mourning doves, Zenaida macroura

Birds are an enigma: their plasma glucose concentration is 1.5–2 times higher than similar-sized mammals, yet they do not normally exhibit symptoms of diabetes. We hypothesized that feeding adult mourning doves a refined carbohydrate diet (white bread: WB) for four weeks would raise plasma glucose concentrations and alter metabolic pathways and endothelial function when compared to birds receiving a nutritionally-balanced diet (bird seeds: SD). Following the four-week long diets, birds were euthanized, and cardiac blood, liver, and pectoralis muscles were collected for metabolomics analyses and biochemical assays. Cranial tibial arteries were dissected to measure acetylcholine-mediated vasodilation. Contrary to the hypothesis, WB-fed birds did not have increased plasma glucose concentrations. Principle component analysis score plots suggest minimal differences between groups. However, we identified 15 changes in individual metabolite concentrations between diet groups that, although not statistically significant, are highly predictive (area under receive operating curve, AUROC>0.90; number of highly predictive metabolites: 5 of 123 in plasma, 4 of 92 in liver, and 6 of 92 in pectoralis muscle). Moreover, pathway analyses revealed no significantly altered metabolic pathways between groups. Biochemical assays revealed no significant group differences in plasma uric acid and insulin, or pectoralis muscle glycogen concentrations. However, hepatic glycogen concentration was 2.12-fold higher in the WB group than in control doves (p = .015). Diet type did not influence vasodilation. In conclusion, a four-week long white bread diet increased liver glycogen but did not alter plasma glucose concentrations, metabolic or vascular physiology in mourning doves.

Xanthophyll β-Cryptoxanthin Inhibits Highly Refined Carbohydrate Diet-Promoted Hepatocellular Carcinoma Progression in Mice.

β-Cryptoxanthin (BCX) can be cleaved by both β-carotene 15,15'-oxygenase (BCO1) and β-carotene 9',10'-oxygenase (BCO2), generating biological active vitamin A and apocarotenoids. We examined whether BCX feeding could inhibit diethylnitrosamine (DEN)-initiated, highly refined carbohydrate diet (HRCD)-promoted hepatocellular carcinoma (HCC) development, dependent or independent of BCO1/BCO2 activity. Two-week-old male wild-type (WT) and BCO1-/- /BCO2-/- double knockout (DKO) mice are given a single intraperitoneal injection of DEN (25mg kg-1 body weight) to initiate hepatic carcinogenesis. At 6 weeks of age, all animals are fed HRCD (66.5% of energy from carbohydrate) with or without BCX for 24 weeks. BCX feeding increases hepatic vitamin A levels in WT mice, but not in DKO mice that shows a significant accumulation of hepatic BCX. Compared to their respective HRCD littermates, both WT and DKO fed BCX have significantly lower HCC multiplicity, average tumor size, and total tumor volume, and the steatosis scores. The chemopreventive effects of BCX are associated with increased p53 protein acetylation and decreased protein levels of lactate dehydrogenase and hypoxia-inducible factor-1α in tumors. This study suggests that BCX feeding may alleviate HRCD-promoted HCC progression by modulating the acetylation of p53, hypoxic tumor microenvironment, and glucose metabolism, independent of BCO1/BCO2.

Dietary β-Cryptoxanthin Inhibits High-Refined Carbohydrate Diet–Induced Fatty Liver via Differential Protective Mechanisms Depending on Carotenoid Cleavage Enzymes in Male Mice

β-Cryptoxanthin (BCX), a provitamin A carotenoid shown to protect against nonalcoholic fatty liver disease (NAFLD), can be cleaved by β-carotene-15,15'-oxygenase (BCO1) to generate vitamin A, and by β-carotene-9',10'-oxygenase (BCO2) to produce bioactive apo-carotenoids. BCO1/BCO2 polymorphisms have been associated with variations in plasma carotenoid amounts in both humans and animals. We investigated whether BCX feeding inhibits high refined-carbohydrate diet (HRCD)-induced NAFLD, dependent or independent of BCO1/BCO2. Six-week-old male wild-type (WT) and BCO1-/-/BCO2-/- double knockout (DKO) mice were randomly fed HRCD (66.5% of energy from carbohydrate) with or without BCX (10 mg/kg diet) for 24 wk. Pathological and biochemical variables were analyzed in the liver and mesenteric adipose tissues (MATs). Data were analyzed by 2-factor ANOVA. Compared to their respective HRCD controls, BCX reduced hepatic steatosis severity by 33‒43% and hepatic total cholesterol by 43‒70% in both WT and DKO mice (P<0.01). Hepatic concentrations of BCX, but not retinol and retinyl palmitate, were 33-fold higher in DKO mice than in WT mice (P<0.001). BCX feeding increased the hepatic fatty acid oxidation protein peroxisome proliferator-activated receptor-α, and the cholesterol efflux gene ATP-binding cassette transporter5, and suppressed the lipogenesis gene acetyl-CoA carboxylase 1 (Acc1) in the MAT of WT mice but not DKO mice (P<0.05). BCX feeding decreased the hepatic lipogenesis proteins ACC and stearoyl-CoA desaturase-1 (3-fold and 5-fold) and the cholesterol synthesis genes 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase and HMG-CoA synthase 1 (2.7-fold and 1.8-fold) and increased the cholesterol catabolism gene cholesterol 7α-hydroxylase (1.9-fold) in the DKO but not WT mice (P<0.05). BCX feeding increased hepatic protein sirtuin1 (2.5-fold) and AMP-activated protein kinase (9-fold) and decreased hepatic farnesoid X receptor protein (80%) and the inflammatory cytokine gene Il6 (6-fold) in the MAT of DKO mice but not WT mice (P<0.05). BCX feeding mitigates HRCD-induced NAFLD in both WT and DKO mice through different mechanisms in the liver-MAT axis, depending on the presence or absence of BCO1/BCO2.

The High Refined Carbohydrate Diet Promotes Renal Injury in Mice Exposed to Cigarette Smoke

The High Refined Carbohydrate Diet Promotes Renal Injury in Mice Exposed to Cigarette Smoke

Diet-related Physiological Plasticity of Mourning Doves: A Metabolomic Approach (P09-002-19)

ObjectivesAs birds are a natural model of diabetes, the objective of this study was to test the hypothesis that feeding adult mourning doves, Zenaida macroura, a high fat diet (60% calories from fat; HF) or refined carbohydrate diet (white bread: WB) for four weeks results in diabetes-like pathologies including hyperglycemia and altered metabolic profiles. MethodsSeparate cohorts of doves were captured for each feeding trial and were acclimated for one week to their respective study diets; cohort 1: WB (n = 6) vs nutritionally-balanced seeds (n = 6), and cohort 2: HF (n = 4) vs control (n = 6). The WB study mimicked natural feeding options for wild birds whereas the HF study used experimental diets. Four weeks later, birds were euthanized with an overdose of sodium pentobarbital and we collected cardiac blood, liver, kidney (HF study only), and pectoralis muscle for metabolomic analyses and biochemical assays. ResultsPathway analysis of metabolic concentrations revealed only two pathways that were significantly altered (p < 0.05) and concurrently highly impacted (scale: 0-1; > 0.60) by the HF diet consumption: ubiquinone and other terpenoid-quinone biosynthesis (plasma and pectoralis muscle) and alanine, aspartate, and glutamate metabolism (plasma and kidney; p < 0.05). Only three low impact pathways were significantly affected by the WB diet consumption: glutathione metabolism and histidine metabolism (liver), and glyoxylate and dicarboxylate metabolism (pectoralis muscle; p < 0.05). Further, consumption neither of the HF nor of the WB diet altered plasma uric acid, insulin, pectoralis muscle, liver triglycerides, or body mass (only measured in HF study) significantly, but liver glycogen concentrations were 2.12-fold higher in WB than control doves (p < 0.015). Lastly, blood glucose concentrations did not differ between WB or HF birds and control birds. ConclusionsContrary to our hypothesis, consumption of a WB or HF diet for four weeks did not induce symptoms of diabetes in doves. Further elucidating the apparent avian resistance to diet-induced metabolic complications may help develop novel therapeutic agents for mammalian diabetes. Funding SourcesASU School of Life Sciences/Office of Knowledge Enterprise Development - Research Investment Initiative, a summer research fellowship from the American Physiology Society, and the Center of Evolution and Medicine Graduate Fellow Award.

Dietary interventions for induction and maintenance of remission in inflammatory bowel disease.

Dietary interventions for induction and maintenance of remission in inflammatory bowel disease.

Consumption of a Refined Carbohydrate Diet Does Not Impair Vasodilation of Cranial Tibial Arteries in the Mourning Dove, Zenaida macroura

Chronic hyperglycemia in mammals correlates positively with the production of reactive oxygen species (ROS) and is associated with impaired vasodilation. Plasma glucose (Pglu) in birds including Mourning Doves (MODO) is generally higher than in mammals, yet vascular ROS in MODO are similar to levels measured in healthy rodents. This difference may be due to abundant endogenous antioxidants such as uric acid and vitamin C in birds. We hypothesized that feeding doves a refined carbohydrate diet would not impair vasodilation. To examine this, we captured MODO (n = 11) in Tempe, AZ, and housed them for five weeks. Birds were acclimated for one week during which they transitioned either to a nutritionally‐balanced dove seed diet (controls, CONT) or to a refined carbohydrate (WB; white sandwich bread) diet. We collected a blood sample from the brachial vein of each bird upon arrival and at the end of the 4‐week treatment for the measurement of serum metabolites. At the end of the study, we euthanized birds and cranial tibial arteries were isolated, cannulated with glass pipettes, and pressurized in a vessel chamber. Isolated arteries were pre‐constricted to 50% of the initial diameter by adding increasing doses of phenylephrine to the superfusate. We then measured vasodilation by adding increasing doses of the endothelium‐dependent vasodilator acetylcholine (10−9 M to 10−5 M). Vasodilation, serum glucose, uric acid, triglycerides, and free glycerol were not significantly different between groups (p&gt;0.05). To examine the effects of captivity, we compared data to those from previous studies on isolated arteries from wild MODO (WILD). Endothelium‐dependent vasodilation was greater in captive than wild doves (CONT vs. WILD, p&lt;0.01; WB vs. WILD, p&lt;0.05). These findings are consistent with our hypothesis as refined carbohydrate consumption did not impair vasodilation. Moreover, captivity improved vasodilation when compared to wild doves regardless of diet type. The findings contrast with those in mammals, in which high carbohydrate consumption results in impaired endothelium‐dependent vasodilation.Support or Funding InformationThis study was funded in part by an IOSP APS summer research fellowship (WC).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The administration of a high refined carbohydrate diet promoted an increase in pulmonary inflammation and oxidative stress in mice exposed to cigarette smoke.

This study aimed to evaluate the effects of a high refined carbohydrate diet and pulmonary inflammatory response in C57BL/6 mice exposed to cigarette smoke (CS). Twenty-four male mice were divided into four groups: control group (CG), which received a standard diet; cigarette smoke group (CSG), which was exposed to CS; a high refined carbohydrate diet group (RG), which received a high refined carbohydrate diet; and a high refined carbohydrates diet and cigarette smoke group (RCSG), which received a high refined carbohydrate diet and was exposed to CS. The animals were monitored for food intake and body weight gain for 12 weeks. After this period, the CSG and RCSG were exposed to CS for five consecutive days. At the end of the experimental protocol, all animals were euthanized for subsequent analyses. There was an increase of inflammatory cells in the bronchoalveolar lavage fluid (BALF) of CSG compared to CG and RCSG compared to CG, CSG, and RG. In addition, in the BALF, there was an increase of tumor necrosis factor alpha in RCSG compared to CG, CSG, and RG; interferon gamma increase in RCSG compared to the CSG; and increase in interleukin-10 in RCSG compared to CG and RG. Lipid peroxidation increased in RCSG compared to CG, CSG, and RG. Furthermore, the oxidation of proteins increased in CSG compared to CG. The analysis of oxidative stress showed an increase in superoxide dismutase in RCSG compared to CG, CSG, and RG and an increase in the catalase activity in RCSG compared with CG. In addition, there was a decrease in the glutathione reduced/glutathione total ratio of CSG, RG, and RCSG compared to CG. Therefore, the administration of a high refined carbohydrate diet promoted an increase in pulmonary inflammation and oxidative stress in mice exposed to CS.

Carbohydrate-enriched diet predispose to anxiety and depression-like behavior after stress in mice

Objectives: Obesity is a chronic disease frequently associated with serious co-morbidities, such as diabetes type II, metabolic syndrome, and psychiatric disorders. Little is known, however, regarding the behavioral consequences of modified diet constituents and the propensity to development of stress related disorders. Thus, the aim of this study was to verify whether chronic exposure to a normocaloric/high-carbohydrate diet will modify the animal's behavior after different stressful stimuli.Methods: BALB/c mice were fed for 12 weeks with a standard chow diet or high refined carbohydrate-containing diet (HC). Following this period, independent groups of animals were exposed to different stress paradigms: 1 – two hours of restraint stress followed by exposure to the Elevated Plus Maze test (EPM) 24 hours later; 2 – The contextual fear conditioning (CFC) test and 3 – the tail suspension test (TST).Results: Despite no change on total body weight, animals fed with HC diet showed increase in serum leptin levels and higher adiposity compared to diet control group. In behavioral tests, animals from HC diet group displayed reduction in the percentage of entries into the open arms of the EPM, evaluated 24 hours after restraint stress, suggesting an anxiogenic-like effect. It is also observed increase in aversive memory in the CFC test and depressive-like behavior in TST.Discussion: Our results suggest that a moderate obesity, induced by high refined carbohydrate diet, may facilitate the development of anxiety and depressive-like behaviors after the stress. The mechanisms responsible for such effects remain to be elucidated.

Inflammatory state of periaortic adipose tissue in mice under obesogenic dietary regimens

High-fat diet or high-sugar diet causes obesity and a chronic low-grade inflammation that leads to the development of diabetes and cardiovascular diseases. Inflammation of the surrounding fat of thoracic aorta namely periaortic adipose tissue (PAAT) has been associated with increased prevalence of vascular diseases in obesity. C57Bl/6 male mice (12 weeks of age) fed a whole grain-based commercial diet (WGD), refined carbohydrate diet (RCD), refined carbohydrate diet plus sweetened condensed milk ad libitum (RCD + CM) or high-fat diet (HFD) for eight weeks were studied. Serum fatty acid (FA) composition was evaluated by gas chromatography. The cellularity (as indicated by DNA and protein contents) and the inflammatory state (as indicated by the contents of TNF-α, IL-6, IL-1β, IL-10, VCAM-1, ICAM-1, leptin and adiponectin measured by ELISA) of the PAAT and thoracic aorta (TA) were evaluated. Both obesogenic regimens (RCD + CM and HFD) increased the content of total fatty acids (FA) in serum and the cellularity of the PAAT compared to WGD. RCD + CM increased serum monounsaturated fatty acid (MUFA) levels and HFD increased serum saturated fatty acid (SFA) levels compared to WGD. RCD (one of the diets used as control) and RCD + CM increased the levels of TNF-α, IL-1β, IL-10 and VCAM-1 in the PAAT compared to WGD. Mice fed with HFD showed decreased contents of TNF-α, VCAM-1 and IL-10 in the PAAT compared to animals fed RCD. The RCD raised the levels of SFA in serum, cellularity and inflammatory state in the PAAT compared to WGD. In conclusion, the effects of obesogenic dietary regimens on PAAT can be interpreted differently when the results are compared with WGD or RCD. We found marked changes in the PAAT and no significant modifications in TA indicating this adipose tissue as the major starting point of vascular diseases.

The Effects of the Combination of a Refined Carbohydrate Diet and Exposure to Hyperoxia in Mice.

Obesity is a multifactorial disease with genetic, social, and environmental influences. This study aims at analyzing the effects of the combination of a refined carbohydrate diet and exposure to hyperoxia on the pulmonary oxidative and inflammatory response in mice. Twenty-four mice were divided into four groups: control group (CG), hyperoxia group (HG), refined carbohydrate diet group (RCDG), and refined carbohydrate diet + hyperoxia group (RCDHG). The experimental diet was composed of 10% sugar, 45% standard diet, and 45% sweet condensed milk. For 24 hours, the HG and RCDHG were exposed to hyperoxia and the CG and RCDG to ambient air. After the exposures were completed, the animals were euthanized, and blood, bronchoalveolar lavage fluid, and lungs were collected for analyses. The HG showed higher levels of interferon-γ in adipose tissue as compared to other groups and higher levels of interleukin-10 and tumor necrosis factor-α compared to the CG and RCDHG. SOD and CAT activities in the pulmonary parenchyma decreased in the RCDHG as compared to the CG. There was an increase of lipid peroxidation in the HG, RCDG, and RCDHG as compared to the CG. A refined carbohydrate diet combined with hyperoxia promoted inflammation and redox imbalance in adult mice.

A historical exploration of Indian diets and a possible link to insulin resistance syndrome

BackgroundInsulin resistance syndrome, especially with diabetes, is becoming increasingly prevalent in India. The increasing consumption of low-fibre and refined carbohydrates is thought to be related to the increased risk of insulin resistance syndrome. AimThe aim was to study the history of eating behaviours in India; the patterns (macronutrients, frequency, and quantity) of food consumption amongst ancient, medieval and modern Indians; and the evolution of a primarily low-fibre and refined-carbohydrate diet. MethodsThe ancient dietary laws of India, historical documents, and ancient and medieval literature and poetry, spanning more than 2000 years, were studied. These data were compared with modern diets among people of different geographical regions, religions and social strata using the National Nutritional Database of the US Department of Agriculture (USDA) for analysis. ConclusionsThe data presented shows a gradual shift over the centuries from the Pastoral Age diet of large quantities of high-fibre carbohydrates, small amounts of digestible carbohydrates, moderate fats, moderate proteins, to an increasing and frequent intake of high-fibre carbohydrates associated with significant drop in protein and fat consumption between 1775 and 1947. From 1947 onwards there has been an increase in the frequency of intake and quantities of low-fibre and refined carbohydrates, and fats with protein intake improving only marginally.

PROSTATIC HYPERPLASIA INDUCED BY HIGH-FAT/HIGH REFINED CARBOHYDRATE DIET

You have accessJournal of Urology1 Apr 2009PROSTATIC HYPERPLASIA INDUCED BY HIGH-FAT/HIGH REFINED CARBOHYDRATE DIET Kevin E McKenna and James B. Young Kevin E McKennaKevin E McKenna More articles by this author and James B. YoungJames B. Young More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(09)61436-1AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "PROSTATIC HYPERPLASIA INDUCED BY HIGH-FAT/HIGH REFINED CARBOHYDRATE DIET." The Journal of Urology, 181(4S), p. 509 © 2009 by American Urological AssociationFiguresReferencesRelatedDetails Volume 181Issue 4SApril 2009Page: 509 Advertisement Copyright & Permissions© 2009 by American Urological AssociationMetricsAuthor Information Kevin E McKenna More articles by this author James B. Young More articles by this author Expand All Advertisement PDF downloadLoading ...

Hepatoprotective effect of Apocynum venetum L extract on fatty liver disease of 2K1C rats with high-fat and refined-carbohydrate diet

Hepatoprotective effect of Apocynum venetum L extract on fatty liver disease of 2K1C rats with high-fat and refined-carbohydrate diet

Developmental origins of obesity: a sympathoadrenal perspective

Environmental exposures at crucial points in development permanently alter sympathoadrenal function in mammals. Both the sympathetic innervation of peripheral tissues and the responsiveness of sympathetic nerves and adrenal medulla to standard stimuli are susceptible to modification by exposures in early life. Several conditions studied in the laboratory, including environmental temperature, litter size and maternal nutrition, in addition to affecting sympathoadrenal function also produce larger, fatter offspring, raising the possibility that developmental programming of the sympathetic nervous system (SNS) may contribute to acquisition of an obese phenotype. The specific changes noted in all three circumstances include evidence of an increase in sympathetic innervation in pancreas and retroperitoneal fat. By contrast, SNS development is impaired in experimental models of intrauterine growth retardation. Although the physiological implications of increased sympathetic innervation in pancreas and retroperitoneal fat are not fully understood, these changes seen in animals reared at cool temperatures, in small litters or by mothers fed refined carbohydrate diets likely reflect an early enhancement of the offspring's capacity to take up and store glucose. If so, the tendency of these animals to gain weight and accumulate fat may represent an adaptive response to 'over-nutrition' in early life.