STD Diet Research Articles

Imaging Non-alcoholic Fatty Liver Disease Model Using H-1 and F-19 MRI.

We explore the use of intravenously delivered perfluorocarbon (PFC) nanoemulsion and 19F MRI for detecting inflammation in a mouse model of non-alcoholic fatty liver disease (NAFLD). Correlative studies of 1H-based liver proton density fat fraction (PDFF) and T1 measurements and histology are also evaluated. C57BL/6 mice were fed standard or high-fat diet (HFD) for 6weeks to induce NAFLD. 1H MRI measurements of PDFF and T1 relaxation time were performed at baseline to assess NAFLD onset prior to administration of a PFC nanoemulsion to enable 19F MRI of liver PFC uptake. 1H and 19F MRI biomarkers were acquired at 2, 21, and 42days post-PFC to assess changes. Histopathology of liver tissue was performed at experimental endpoint. Significant increases in liver volume, PDFF, and total PFC uptake were noted in HFD mice compared to Std diet mice. Liver fluorine density and T1 relaxation time were significantly reduced in HFD mice. We demonstrated longitudinal quantification of multiple MRI biomarkers of disease in NAFLD mice. The changes in liver PFC uptake in HFD mice were compared with healthy mice that suggests that 19F MRI may be a viable biomarker of liver pathology.

The effect of metformin on cardiovascular markers in female mice consuming a high fat diet

BackgroundMetformin, widely used to treat diabetes, is now considered a candidate therapeutic for treatment of cardiovascular disease. This study aimed to assess whether metformin’s non-glycaemic effects could mitigate cardiovascular disease indices in female mice consuming a high fat diet (HFD). MethodsFour-week old female Arc:Arc(S) mice were placed on a standard (std) chow diet or Western-style HFD (22% fat, 0.15% cholesterol). At ∼8 months, the mice were administered 150 mg/kg metformin or vehicle (control) via intraperitoneal injection for 11 days. Blood pressure was measured (tail cuff plethysmography) at Day 9 and 11 of treatment. On Day 11, mice were weighed and culled. The mesenteric arcade and kidneys were collected for assessment of vascular reactivity (wire myography), and assessment of expression of cardiometabolic markers (qPCR), respectively. ResultsThe HFD fed female mice were significantly heavier than those receiving the std diet at 1–12 weeks on diet, and at cull. Mice on a std diet with metformin treatment were significantly heavier at cull than the mice on a std diet administered the control treatment. Metformin treatment did not alter the weight of the mice receiving the HFD. Neither the HFD (compared to the std diet), nor metformin treatment (compared to control treatment) altered blood pressure, vascular reactivity, or expression of cardiometabolic markers in the kidney. ConclusionConsumption of a Western-style HFD (without high salt/sugar levels) did not alter the cardiovascular markers measured. Further studies are required to establish the non-glycaemic, cardio-protective effects of metformin in high-risk cohorts.

Temperature and Temperature Humidity Index Changes during Summer to Autumn in a Temperate Zone May Affect Liveweight Gain and Feed Efficiency in Sheep

Lamb finishing during summer in southern Australia faces the challenges of dry paddock feed of low nutrient value and energy concentration, combined with periods of high temperature that reduce appetite. One potential forage to overcome these challenges is camelina, a brassica with a high lipid concentration. Liveweight gain (LWG) and feed efficiency (FE) of a pelleted diet containing 15% camelina hay (CAM) were compared with an equivalent diet based on oaten hay (STD), a feed commonly used during dry seasons. The experiment was conducted under summer to autumn conditions using 56 maternal Composite (Composite) wether lambs (4 months, 28–38 kg liveweight) and 56 Merino wether yearlings (15 months, 37–43 kg liveweight). Animals were maintained in group pens (8/pen) and weekly average feed intakes per pen and liveweights per pen were determined in a shaded well-ventilated animal house. The LWG and FE for both animal types were significantly lower during weeks 5–8 compared with weeks 1–4. These changes coincided with a higher proportion of daytime maxima exceeding 28 °C (50% vs. 21%) and night-time hours exceeding 22 °C (15% vs. 9%). The experiment indicated that the LWG and FE of sheep fed the CAM diet were less affected by the elevated temperatures than sheep fed the STD diet during weeks 5–8. However, further research under controlled environmental conditions is required to further validate these results.

Improved fillet quality in harvest-size Atlantic salmon fed high n-3 canola oil as a DHA-source

New sources of the very long-chain n-3 polyunsaturated fatty acids (n-3 VLC-PUFA) are needed for sustainable growth of salmon farming. In recent research high n-3 VLC-PUFA canola oil has shown promise as a safe and effective source of docosahexaenoic acid (DHA) and other n-3 PUFA in small Atlantic salmon. To study its long-term effects on performance and fillet quality under realistic farming conditions, a 12-month feeding experiment was carried out with Atlantic salmon growing to harvest weight (4.7 kg) in triplicate sea water cages. The fish were fed three diets containing graded inclusion levels of high n-3 canola oil resulting in levels of dietary DHA (22:6 n-3) of 4.0% (Standard; STD), 6.6% (Medium; MED) and 8.3% of total fatty acids (HIGH) and total EPA + DHA of 6.4, 9.1 and 11.0% of total fatty acids, respectively. The STD diet was considered to represent current commercial practice. There were no significant differences between the dietary groups in overall fish growth and weight at harvest, and no differences were seen in feed conversion ratio. Tissue FA-profiles mirrored the diets, giving increased DHA, EPA (20:5 n-3) and ALA (18:3 n-3) with increasing inclusion level of high n-3 LC-PUFA canola oil. Dietary inclusion of n-3 canola oil had no effect on muscle astaxanthin concentration, but instrumentally measured redness, yellowness and chroma increased with n-3 canola oil inclusion, suggesting a positive effect on colour via effects on muscle structure or composition. The prevalence and severity of dark melanin spots in the fillet was significantly reduced by increased inclusion level of n-3 canola oil. The prevalence of severe spots (score ≥ 2), average score and number of affected muscle segments were all lower in MED and HIGH, compared to STD.In conclusion, high n-3 canola oil is an efficient source of DHA and other n-3 fatty acids for harvest-size Atlantic salmon. Increased dietary supply of DHA and other n-3 PUFA, above minimum requirement levels for DHA, improved fillet pigmentation and reduced fillet melanin spots, without compromising fish growth.

Eruca sativa Mill. seed extract promotes anti-obesity and hypoglycemic effects in mice fed with a high-fat diet.

Obesity is currently considered a major source of morbidity, with dramatic complications on health status and life expectancy. Several studies demonstrated the positive effects of Brassicaceae vegetables on obesity and related diseases, partially attributing these beneficial properties to glucosinolates and their derivatives isothiocyanates. Recently, isothiocyanates have been described as a hydrogen sulfide (H2 S)-releasing moiety, suggesting that H2 S may be at least in part responsible for the beneficial effects of Brassicaceae. In this work, the metabolic effects of an extract obtained from Eruca sativa Mill. seeds (E.S., Brassicaceae), containing high levels of glucoerucin, were evaluated in an experimental model of obesity. Male balb/c mice were fed for 10 weeks with standard (Std) diet or high fat (HF) diet supplemented with E.S. E.S. significantly contained the body weight gain in this obesity model, improving also glucose homeostasis. Interestingly, lower values of white adipose tissue mass and a significant reduction of adipocytes size were also observed. Moreover, E.S. enhanced the adipocytes metabolism, improving the citrate synthase activity and reduced triglyceride levels in mice fed with HF diet. Taken together, these results suggest that E.S. is endowed with an interesting translational and nutraceutical value in the prevention of metabolic disorders, suggesting that H2 S could be a key player.

A high-fat diet rich in corn oil exaggerates the infarct size and memory impairment in rats with cerebral ischemia and is associated with suppressing osteopontin and Akt, and activating GS3Kβ, iNOS, and NF-κB.

The increase in osteopontin (OPN) levels after stroke induces neural protection by activating Akt signaling and inhibiting GS3Kβ, iNOS, and NF-κB. This study investigated the effect of a high-fat diet rich in corn oil (CO-HFD) on infarct size and memory function in rats after induction of cerebral ischemia in rats and investigated its effect on the expression of OPN/Akt/iNOS/NF-κB signaling pathways. Rats were initially fed a standard diet (STD, 3.82kcal/g; 9.4%, from fat) or a CO-HFD (5.4kcal/g, 40% from fat) for 12weeks. Then, both groups were further subdivided into either sham group or group exposed to cerebral ischemia by the middle cerebral artery occlusion (MCAO) protocol. Compared with sham-operated rats fed STD diet, neurological scores and both short- and long-term memory functions were significantly impaired in sham-operated CO-HFD-fed rats. In addition, brains collected from CO-HFD-fed rats showed lower protein levels of OPN, p-Akt (Thr308), p-GS3Kβ (Ser9), and Bcl-2 and had higher protein levels of iNOS, cleaved caspase-3, nuclear NF-κB p65, and cytoplasmic cytochrome C. However, once exposed to MCAO surgery, similar but more profound alterations of all these biochemical parameters with more severe impairment in short- and long-term memory functions and larger infarct size were noticed in the brains of CO-HFD-fed rats as compared with STD-fed rats exposed to MCAO. In conclusion, chronic consumption of CO-HFD induces memory impairments and worsens memory function recovery and infarct size after cerebral ischemia in rats by reducing levels of OPN, inhibiting the activation of Akt and activating iNOS and NF-κB.

Effects of RVD-hemopressin (α) on feeding and body weight after standard or cafeteria diet in rats

Palatability and variety of foods are major reasons for hedonic eating, and hence for obesity. Hemopressin, a hemoglobin α chain-derived peptide, plays antagonist/inverse agonist role on cannabinoid (CB)1 receptors, while RVD-hemopressin(α)[RVD-hp(α)], a N-terminally extended form of hemopressin, has been reported as an allosteric modulator of CB1 and CB2 receptors.We investigated the effects of 14 daily intraperitoneal injections of RVD-hp(α), in Sprague-Dawley rats fed a highly palatable cafeteria-style (CAF) diet (30% fat, 56% carbohydrate, 14% protein; 4.20 kcal/g) compared to standard laboratory chow (STD) food (3.5% fat, 63% carbohydrate, 14% protein, 19.5% other components without caloric value; 3.20 kcal).Food intake, body weight and locomotor activity were recorded throughout the study. Finally, rats were sacrificed and agouti-related peptide (AgRP), neuropeptide Y (NPY), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real-time reverse transcription polymerase chain reaction.We found that CAF diet increased food intake as compared to STD diet. In both STD and CAF diet fed rats, RVD-hp(α) treatment inhibited food intake, increased locomotor activity but did not modify body weight. In vehicle injected animals, CAF as compared to STD diet increased AgRP gene expression. RVD-hp(α) treatment decreased POMC mRNA levels in both diet groups and lowered the elevated AgRP levels induced by CAF diet.RVD-hp(α) treatment plays an anorexigenic role paralleled by increased locomotor activity both in STD and CAF diet fed rats. The inhibition of feeding could be partially mediated by lowering of hypothalamic POMC and AgRP gene expression levels.

The choice of animal feeding system influences fatty acid intakes of the average French diet

Fatty acids intake of French adult population does not comply with the French Population Reference Intakes (PRI). The aim the study is to quantify the impact of a modification of animal feeding system on the fatty acids intake of French population. A 15-day diet representative of average consumption for the French adult male population was developed with animal products derived either from conventional production system (STD) either from a specific production system (Bleu-Blanc-Cœur®[BBC]) that acts on the fatty acids profile of animal products. The impact of a such change in feeding system on fatty acids content has been quantified. BBC diet contributes to reducing the gap between the fatty acid content of a STD diet and the PRI with highest impact on C12:0–14:0–16:0 fatty acids (−4.6 g/d,i.e.63.3%), C18:3n-3 (+0.8 g/d,i.e.48.2%), C20:5n-3 (+35 mg/d,i.e.42.7%), C22:6n-3 (+49 mg/d,i.e.35%) and the C18:2n-6/C18:3n-3 ratio (−4.9 points,i.e.43.5%). The research also shows that animal products complement one another. Consuming a variety of animal source foods derived from a specific feeding practices could help reduce the gap between actual consumption and recommended dietary intake of fatty acids.

Effects of Ketogenic Diet in Young Adult and Old Rats

Ketogenic diets (KD) have been promoted extensively for weight loss and health. However, their effects in aged skeletal muscle are not well‐defined. In this study, we tested the effect of a ketogenic diet in young adult (YA; 5 month old) and old (O; 28 month old) male Fisher 344 rats (n = 4–6/group). Rats were assigned to either standard chow (STD; Evigo Teklad Rodent Diet, 8604; 32% protein, 14% fat, 54% carbohydrate) or ketogenic diet (KETO; Envigo Teklad Custom Diet, TD.10911; 22.4% protein, 77.1% fat, 0.5% carbohydrate) for 4 weeks, and weighed weekly. KETO rats were pair fed isocalorically with STD chow rats within each age group with the YA rats eating 0.132 kcal/g body weigh/day, and O rats eating 0.109 kcal/g body weight/day. After 24 or 25 days glucose tolerance testing was performed by fasting the rats for 6 hours followed by an injection of 1 mg glucose/g BW. Blood glucose concentration was measured from tail blood immediately before and 15, 30, 60 and 120 minutes after the glucose injection. Ketones were also measured from tail blood immediately before the glucose injection. After the 4‐week treatment period, rats were euthanized and gastrocnemius muscle was collected for determination of mitochondrial respiration and AMP‐activated protein kinase (AMPK; an important stimulator of glucose and fatty acid metabolism) phosphorylation. We found that KETO feeding increased blood ketone levels, albeit non‐significantly (p=0.065), in YA but not O rats. KETO resulted in significant weight loss within 2 weeks in both YA and O rats. Glucose tolerance was impaired in O‐STD vs. YA‐STD rats, while KETO impaired glucose tolerance in YA, but not O rats. KETO increased mitochondrial respiration in YA, but not O rats. AMPK phosphorylation was decreased by KETO vs. STD diet in YA, but not O rats. We conclude that a KETO diet induces a significant drop in body weight and enhanced mitochondrial respiration, but impaired glucose tolerance in YA rats, suggesting a shift from glycolytic to oxidative metabolism. Somewhat surprisingly, these KETO‐induced changes in YA rats are associated with decreased AMPK activation. O rats are resistant to all of these effects of KETO diet except for weight loss, suggesting impaired metabolic plasticity with old age. Further study will be required to elucidate the exact molecular pathways underlying these shifts.Support or Funding InformationThis research was supported by Brigham Young University Mentoring Environment Grants (MEG) and Gerontology Research Grants.

Prolonged high altitude exposure exacerbates fat‐free mass and fat mass loss during negative energy balance regardless of dietary protein intake

Protein intake above the recommended dietary allowance attenuates fat‐free mass (FFM) loss during moderate negative energy balance (~40% energy deficit) at sea level (SL). Sustained periods of strenuous physical activity at high altitude (HA) may exacerbate FFM loss, especially during energy deficit. However, increased dietary protein intake has not been evaluated as a countermeasure to FFM loss at HA. This study aimed to determine whether consuming dietary protein at amounts consistent with current recommendations for elevated physical activity (2.0 g protein/kg) attenuates FFM loss during prolonged energy deficit at HA. Seventeen healthy males (mean ± SD, 23.4 ± 5.6y, 81.9± 13.9 kg) participated in a 2‐phase, 43‐d study. During phase 1 (SL), participants were instructed to consume a weight maintenance diet with standard protein intake(1.0 g protein/kg, STD) for 21 d. During phase 2, participants resided at HA (4300 m, Pikes Peak, CO) for 22 d and were randomly assigned to either a STD or high (2.0 g protein/kg, HIGH) protein diet designed to elicit a 40% energy deficit (30% dietary restriction and 10% increase in physical activity, estimated energy deficit was 1074 ± 122 kcal/d based on the total energy requirements necessary to maintain body mass during phase 1) and~3 kg total body mass loss. Diet and physical activity were highly controlled. Total body mass, FFM, and fat mass (FM) were assessed by dual energy x‐ray absorptiometry and resting metabolic rate (RMR) by indirect calorimetry. Volunteers were weight stable during SL and lost −7.9 ± 1.9 kg(P<0.01)during HA, regardless of protein group (P>0.05). Decrements in FFM (−4.0 ± 3.3 vs. −3.2 ± 1.5 kg) and FM (−3.3 ± 1.8 vs. −3.9 ± 0.8 kg) were not statistically different between STD and HIGH (P>0.05). The overall energy deficit was 2306 ± 444kcal/d when calculated based on changes in FFM and FM. The additional energy deficit was attributable, in part, to an increase in RMR, which peaked at 58%above SL on HA day 1 and remained ≥ 25% higher than SL throughout HA(P<0.05), accounting for 27% (634 ± 273 kcal/d) of the total energy deficit at HA. The remaining 598 kcal/d (26% of total deficit) could not be accounted for by estimated energy expenditure of prescribed daily physical activity and measured energy intake, suggesting the energy cost of physical activity may be greater at HA than SL. Prolonged HA exposure exacerbated the catabolic effects of negative energy balance. In this context, consuming a higher versus standard protein diet was equally ineffective at sparing FFM with weight loss. The opinions or assertions contained herein are the private views of the author(s)and are not to be construed as official or reflecting the views of the Army or the Department of Defense.Support or Funding InformationSupported by USAMRMC.

Age-related periodontitis and alveolar bone loss in rice rats

ObjectiveTo characterize in rice rats: (a) periodontitis (PD) progress with feeding of standard laboratory rat chow (STD) during ages 4–80 weeks; and (b) PD progress with feeding of a high sucrose-casein (H-SC) diet during young adulthood. MethodsOne group (N=12) was euthanized at age 4 weeks (Baseline). Four groups (N=8-16) consumed a STD diet from baseline and were necropsied at ages 22, 30, 52, and 80 weeks. Three groups (N=10-16) consumed an H-SC diet from baseline. Two were necropsied at ages 22 and 30 weeks, respectively. The third switched to the STD diet at age 22 weeks and was necropsied at age 30 weeks. All mandibles/maxillae were assessed by histometry for degree of periodontal inflammation (PD Score), alveolar crest height (ACH, mm), and horizontal alveolar bone height (hABH, mm2). ResultsIn STD diet rats aged ≥30 weeks, all endpoints were worse (P<0.05) than at Baseline. In H-SC diet rats aged ≥22 weeks, all endpoints were worse than at Baseline (P<0.05). At age 22 weeks, all endpoints were worse in the H-SC group than in the STD group (P<0.05). By age 30 weeks, the STD and H-SC groups did not differ. Conclusions1) STD diet fed rice rats develop moderate/severe PD by age 30 weeks; 2) an H-SC diet accelerates moderate/severe PD development; and 3) switching to a STD diet does not halt/reverse PD that was accelerated by an H-SC diet. These data further clarify use of the rice rat as a PD model.

Creosote Bush (Larrea tridentata) Improves Insulin Sensitivity and Reduces Plasma and Hepatic Lipids in Hamsters Fed a High Fat and Cholesterol Diet.

Creosote bush, Larrea tridentata (Sesse y Moc. Ex DC, Zygophyllaceae) is a shrub found in the deserts of Northern Mexico and Southwestern United States. In traditional medicine, it is used to treat a variety of illnesses including type 2 diabetes. The present study aims to investigate the effects of creosote bush ethanolic extract on plasma and liver parameters associated with the metabolic syndrome in hamsters fed a high fat and cholesterol diet (HFD), comparing them with those induced by ezetimibe (EZ). Seven groups of six hamsters each were formed. Six groups were fed HFD for 2 weeks. The following 2 weeks, the HFD groups received: (1) only HFD, (2) HFD + 3 mg% EZ, (3) HFD + 0.2% creosote bush ethanolic extract, (4) only standard diet (Std Diet), (5) Std Diet + 3 mg% EZ, (6) Std Diet + 0.2% creosote bush ethanolic extract. The beneficial effects of creosote bush ethanolic extract in the HFD hamster model were a reduction of insulin resistance, associated with lower serum insulin and leptin, lower hepatic lipid peroxidation and higher liver antioxidant capacity. Plasma and liver lipids tended or were reduced to values closer to those of animals fed standard diet. A similar effect on lipids was induced by EZ, although with even lower hepatic cholesterol and total lipids concentrations. In general, the change from HFD to standard diet plus ethanolic extract induced the same but deeper changes, including a reduction in plasma glucose and an increase in the percentage of HDL cholesterol. Unlike creosote bush extract, EZ increased food consumption and neutral fecal steroids, with no significant effect on body weight, epididymal fat pads, liver peroxidation or antioxidant capacity. Also EZ did not modify serum insulin and leptin. However, insulin sensitivity improved to values similar to those induced by the extract. This suggests that the mechanism of action of creosote bush ethanolic extract is different to inhibition of cholesterol absorption or increase excretion. The ethanolic extract of L. tridentata could be useful in the treatment of the metabolic syndrome.

The Association of Malnutrition and Chronic Stress Models Does Not Present Overlay Effects in Male Wistar Rats

Chronic stress and protein-energy malnutrition (PEM) are both social problems resulting in physiological and behavioral alterations. In this present study an associative effects of PEM and chronic stress were evaluated through in Wistar rats. Four groups were established: standard diet– 19% of protein (Std); Std + stress; PEM–6% of protein and PEM + stress. In these groups were assessed physical, nutritional, hematological, histological parameters and anxiety-like behavior. There were a reduction of food intake, body mass and relative weight of the heart and thymus in the PEM group. The liver of the PEM animals presented a degenerative condition with steatosis and Kupffer cell hypertrophy and, additionally, a significant decrease in hematocrit percentages, in the number of red blood cells and in the concentration of hemoglobin and total protein. In those animals under stress and Std diet, there was observed an increase of the relative adrenal weights, an acute condition of leukocytosis with a predominance of neutrophils and an increase in the anxiety-like behavior. There was no overlapping/interaction among the anthropometric, biochemical, hematological and histological effects using PEM and stress in Wistar rats. The effects observed under experimental condition were those related to either PEM or stress, independently.

Effects of a eucaloric reduced-carbohydrate diet on body composition and fat distribution in women with PCOS

ObjectiveTo determine if consumption of a reduced-carbohydrate (CHO) diet would result in preferential loss of adipose tissue under eucaloric conditions, and whether changes in adiposity were associated with changes in postprandial insulin concentration. MethodsIn a crossover-diet intervention, 30 women with PCOS consumed a reduced-CHO diet (41:19:40% energy from CHO:protein:fat) for 8weeks and a standard diet (55:18:27) for 8weeks. Body composition by DXA and fat distribution by CT were assessed at baseline and following each diet phase. Insulin AUC was obtained from a solid meal test (SMT) during each diet phase. ResultsParticipants lost 3.7% and 2.2% total fat following the reduced-CHO diet and STD diet, resp. (p<0.05 for difference between diets). The reduced-CHO diet induced a decrease in subcutaneous-abdominal, intra-abdominal, and thigh-intermuscular adipose tissue (−7.1%, −4.6%, and −11.5%, resp.), and the STD diet induced a decrease in total lean mass. Loss of fat mass following the reduced CHO diet arm was associated with lower insulin AUC (p<0.05) during the SMT. ConclusionsIn women with PCOS, consumption of a diet lower in CHO resulted in preferential loss of fat mass from metabolically harmful adipose depots, whereas a diet high in CHO appeared to promote repartitioning of lean mass to fat mass.

Favourable metabolic effects of a eucaloric lower‐carbohydrate diet in women with PCOS

Diet-induced reduction in circulating insulin may be an attractive nonpharmacological treatment for women with polycystic ovary syndrome (PCOS) among whom elevated insulin may exacerbate symptoms by stimulating testosterone synthesis. This study was designed to determine whether a modest reduction in dietary carbohydrate (CHO) content affects β-cell responsiveness, serum testosterone concentration and insulin sensitivity in women with PCOS. In a crossover design, two diets ('Standard,' STD, 55:18:27% energy from carbohydrate/protein/fat; lower-carbohydrate, 41:19:40) were provided for 8weeks in random order with a 4-week washout between. Thirty women with PCOS. β-cell responsiveness assessed as the C-peptide response to glucose during a liquid meal test; insulin sensitivity from insulin and glucose values throughout the test; insulin resistance (HOMA-IR); and total testosterone by immunoassay. Paired t-test indicated that the lower-CHO diet induced significant decreases in basal β-cell response (PhiB), fasting insulin, fasting glucose, HOMA-IR, total testosterone and all cholesterol measures, and significant increases in insulin sensitivity and dynamic ('first-phase') β-cell response. The STD diet induced a decrease in HDL-C and an increase in the total cholesterol-to-HDL-C ratio. Across all data combined, the change in testosterone was positively associated with the changes in fasting insulin, PhiB and insulin AUC (P<0·05). In women with PCOS, modest reduction in dietary CHO in the context of a weight-maintaining diet has numerous beneficial effects on the metabolic profile that may lead to a decrease in circulating testosterone.

High fat intake with monounsaturated fatty acids, but not n6 polyunsaturated fatty acid, increases activity of key mitochondrial oxidative enzymes in the heart

Evidence suggests that a high fat intake may be beneficial for cardiovascular health, though optimal dietary fatty acid composition is unclear. In this study, we compare the effects of a standard low fat diet (STD, 15% energy from fat) to high fat diets (40% energy from fat) comprised of monounsaturated fat (MUFA, oleate (18:1)), n6 polyunsaturated fat (PUFA, linoleic acid (18:2n6)), or saturated fat (SAT, palmitate and stearate (16:0 and 18:0)). Male rats (n=13–14/group) were fed the STD diet until 16 weeks of age and then assigned to dietary treatment for 15 weeks. Cardiac function was assessed by echocardiography and left ventricle (LV) pressure measurements and was unaffected by diet. Mitochondria were isolated from the LV and show no impact of dietary treatment on mitochondrial yield or respiration with lipid and nonlipid substrates. Mitochondrial oxidative enzyme activity in whole tissue dramatically increased with MUFA compared to STD. Citrate synthase activity increased from 105±15 μmol/g/min in STD to 157±14 in MUFA (P&lt;0.05 vs STD and PUFA), with no significant effect in PUFA (107±9) or SAT (130±11). Similar changes occurred with aconitase and long chain acyl‐CoA dehydrogenase activities. In summary, a high fat diet did not adversely impact cardiac function, increased activity of mitochondrial oxidative enzymes of the TCA cycle and fatty acid oxidation, and did not affect mitochondrial function.

Dietary fat level affects tissue iron levels but not the iron regulatory gene HAMP in rats

Because dietary fats affect the regulation and use of body iron, we hypothesized that iron regulatory and transport genes may be affected by dietary fat. A model of early-stage I to II, nonalcoholic fatty liver was used in which rats were fed standard (35% energy from fat) or high-fat (71% energy from fat) liquid diets with normal iron content (STD/HF groups). In addition, intraperitoneal injections of iron dextran were given to iron-loaded (STD+/HF+ groups) and iron-deficient diets to STD−/HF− groups. Plasma osmolality, hemoglobin level, and mean corpuscular hemoglobin concentration were increased in all STD diet groups compared with all HF diet groups. Plasma iron and transferrin saturation were affected by an interaction between dietary fat and iron. They were high in the STD group (normal iron) compared with their respective HF group. Similarly, this group also showed a 4-fold increase in the messenger RNA expression of the hepatic hemochromatosis gene. Spleen iron was high in the iron-loaded STD+ group compared with all other groups. Hepatic iron and messenger RNA expression of peroxisome proliferator–activated receptor-γ, CCAAT/enhancer binding protein α, interleukin-6, and iron transport genes (transferrin receptor 2, divalent metal transporter 1 iron-responsive element, and divalent metal transporter 1 non–iron-responsive element) were increased, whereas tumor necrosis factor α was decreased in the HF diet groups. The expression of iron regulatory gene HAMP was not increased in the HF diet groups. Iron regulatory and transport genes involved in cellular and systemic iron homeostasis may be affected by the macronutrient composition of the diet.

The effects of a low vitamin E diet on dichloroacetate‐ and trichloroacetate‐induced oxidative stress in the livers of mice

Groups of mice were fed either a standard (Std) diet or a diet not supplemented with vitamin E (Low-E) and were divided into three subgroups that were treated subchronically by gavage, with water (control), dichloroacetate (DCA), or trichloroacetate (TCA). The livers of the animals were assayed for various biomarkers of oxidative stress (OS), antioxidant enzyme activities, and total glutathione (GSH). In general, livers from the low-E diet group expressed lower levels of biomarkers of OS associated with greater increases in various antioxidant enzymes activities and GSH when compared with the corresponding treatments in the Std diet group. These results suggest that vitamin E supplementation to the diet, while essential to maintain certain body functions, can compromise the effectiveness of the hepatic antioxidant enzymes and GSH resulting in an increase in DCA- and TCA-induced OS and a possible increase in the compounds-induced hepatotoxic/hepatocarcinogenic effects in mice.

Vitamin E restriction in the diet enhances phagocytic activation by dichloroacetate and trichloroacetate in mice

The effects of a Vitamin E-restricted diet on the induction of phagocytic activation by dichloroacetate (DCA) and trichloroacetate (TCA) was investigated. Groups of B6C3F1 male mice were either kept on standard diet (Std diet group) or diet that had the vitamin provided only by its natural ingredients (Low-E diet group). The animals in each diet group were administered 77mg of DCA or TCA/ kg/day, or 5ml/kg water (controls), by gavage, for 13weeks. Thereafter, peritoneal lavage cells (PLC) were assayed for superoxide anion (SA), tumor necrosis factor (TNF)-α, and myeloperoxidase (MPO), as well as for the activities of the anti-oxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). SA and TNFα production, as well as MPO, SOD, CAT and GSH-Px activities were significantly increased in the cells from the Low-E diet group treated with the compounds as compared with cells from hosts in the Std-diet group that received the corresponding treatments. The results indicate that consumption of a Vitamin E-restricted diet enhances the induction of phagocytic activation by DCA and TCA, a mechanism that was previously suggested to be an initial adaptive/protective response against the compounds long-term effects.

N-3 PUFA-Enriched Diet Delays the Occurrence of Cancer Cachexia in Rat With Peritoneal Carcinosis

The aim of this study was to evaluate the effects of a fish oil (FO) diet (rich in long chain, n-3, polyunsaturated fatty acid) on cancer cachexia symptoms in rats. To this end, peritoneal carcinosis (PC) was generated by an intraperitoneal injection of cancer cells in BDIX rats fed FO or standard (Std) diets. Food intake and body weight were recorded throughout the study until sacrifice. PC rats were sacrificed when food intake was significantly and severely reduced. Fat and skeletal muscles masses were weighed and serum inflammatory cytokines concentration measured at sacrifice. Occurrence of anorexia in PC rats was delayed in the FO diet group (median time was multiplied by 2.5) in comparison with Std diet. At the time of sacrifice, PC rats displayed a lower body weight gain as well as lower muscle and fat masses than pair-fed rats, suggesting the presence of a hypermetabolism state. Serum TNF-α was significantly increased in PC rats compared with controls rats. There was no effect of FO diet on tissue mass (skeletal muscle and fat) or on TNF-alpha concentration. In conclusion, FO diet delays the appearance of anorexia induced by PC in rats.