Manipulation Of Macronutrients Research Articles

Ergogenic aids: nutrition

It has been an endless pursuit of sportspersons and coaches to adopt various means to boost performance. Anything perceived to have a potential benefit is readily tried with a hope...

The effects of two different hypocaloric diets on glucagon-like peptide 1 in obese adults, relation with insulin response after weight loss

Objective Few studies have investigated the effect of type of diets on GLP-1 concentrations. The aim of this study was to compare the effect of two diets on circulating GLP-1 levels and the relation with insulin response after weight loss. Methods A population of 118 obese patients were analyzed. Patients were randomly allocated to two groups: (a) Diet I (low carbohydrate) and (b) Diet II (low fat). Biochemical and anthropometric parameters were measured before and after 3 months of hypocaloric diet. Results Fifty-two patients (12 male/40 female) were treated with Diet I and 66 patients (21 male/45 female) with Diet II. In Group I, basal GLP-1 levels did not change after dietary treatment (9.4±3.3 vs. 9.9±3.1 ng/ml; ns). In Group II, GLP-1 levels decreased significantly (8.4%) (9.2±3.3 vs 8.7±3.1 ng/ml; P<.05). In the multivariate analysis with a dependent variable (levels of GLP-1), only insulin levels remained as an independent predictor in the model ( F=5.9; P<.05), with an increase of 0.6 ng/ml (95% CI 0.1–1.1) GLP-1 concentrations with each increase of 1 mUI/ml of insulin. Conclusion A hypocaloric diet with a low fat percentage decreased GLP-1 levels with a direct correlation with insulin levels. Nevertheless, patients with a hypocaloric diet with a low carbohydrate percentage treatment did not change GLP-1 levels. Diet macronutrient manipulation on GLP-1 response could be useful in an obesity nutrition therapy.

M1956 Bimodal Effects of Dietary Macronutrient Manipulation On Carcinogenesis in Barrett's Mucosa

INTRODUCTION: Reflux& being overweight are strong risk factors for esophageal adenocarcinoma (EAC). There is a trend toward Low-Carb (LC) diet use among both obese & healthy individuals. The LC diet reduces weight, improves insulin resistance, may decrease reflux & potentially decrease risk of EAC. However, we previously found that LC diet increased levels of procarcinogenic bile salt deoxycholic acid (DCA) in rats. Our AIM was to examine the effect of LC diet on procarcinogenic signaling in Barrett's mucosa & EAC development in rats with reflux. METHODS: Sprague-Dawley rats (n=65) were operated to induce gastroduodenal reflux & randomized at 22 weeks post-op (time to develop Barrett's). The effect of LC diet on procarcinogenic signaling in Barrett's was tested in a short term investigation involving 20 rats randomized (1:1) to LC or balanced (ADA) diet for 4 weeks. The effect of LC diet on development of EAC was examined in a long-term study involving 45 rats randomized (1:2) to LC or ADA diet for 20 weeks. Rats were sacrificed & esophageal tissue tested for PGE2 levels & key enzymes (cPLA2, COX-2) involved in PGE2 synthesis. Presence of Barrett's mucosa & EAC was noted. Serum IGF1 levels & animal weight was examined. RESULTS: The 4 week short-term LC diet significantly increased PGE2 levels (245±41 vs 95±22pg/mg, p=0.002), cPLA2 & COX-2, compared to ADA diet. As seen previously, LC diet increased levels of DCA. In-vitro assays showed that increasing DCA levels up-regulated cPLA2, increased COX-2 & induced PGE2 synthesis. LC diet was associated with weight loss but serum IGF1 levels were not different. Based on these results, we anticipated that up-regulation of carcinogenic signaling with LC diet would increase the rate of EAC. However, the rate of EAC was not different in long-term LC vs ADA rats (9/15, 60% vs 19/30, 63% p=1.0). The long-term LC diet did result in significant weight reduction (321±28gms vs 396±11gms, p=0.03) & lower IGF-1 levels(10±3 vs 1.2±1 ng/ml, p=0.02) compared to ADA diet. CONCLUSIONS: Short-term LC diet supplementation promotes procarcinogenic signaling involving PGE2 synthesis. However, this does not translate to an increased risk of EAC with long-term LC diet supplementation. A possible explanation for the bimodal effect of LC diet is the marked weight reduction & low IGF1 levels with long-term LC diet, which may negate the effects of procarcinogenic signaling. This is clinically relevant because most people use Low-Carb diet for short term rather than long term, which may increase their risk of EAC. Studies to examine the opposing effects of IGF-1/weight reduction & PGE2 pathway are currently being investigated.

The Effect of Pre-Exercise Dietary Manipulation on ATP Utilisation and Metabolism During Simulated Duathlon Performance

Duathlon is a multi-sport event that has received little attention in terms of dietary intervention studies but presents an ideal form of exercise in which the development of appropriate nutritional strategies might benefit performance. PURPOSE: This study investigated the effect of high carbohydrate and high fat meals on the metabolic responses to simulated duathlon time trials. METHODS: Nine male subjects of mean (SD) age 28.6 (5.9) y, body mass 76.8 (8.5) kg, height 1.80 (0.7) m, and VO2max4.8 (0.6) 1.min-1 completed three laboratory simulated duathlon time trials (5 km run, 30 km cycle, and 5 km run). Subjects fasted overnight before each duathlon and were randomly given isoenergetic meals (3998±2.2kJ) 3.5 hours before the start of exercise. The meals consisted of predominantly low carbohydrate (LCHO: 50 g), high carbohydrate (CHO: 214.8 g) or a fasting (F) condition, in which subjects ate nothing. Respiratory gas analysis was used to calculate substrate oxidation rates (Frayn 1983) and ATP utilisation was calculated using standard stoichiometric calculations. Significant differences in all of the data between conditions and over time were identified using a General Linear Model ANOVA with Repeated Measures and significance was accepted at p< 0.05. RESULTS: Time to complete the duathlon (101.9±6.8, 101.0±7.1, 102.4±7.1 min for the F, CHO and LCHO respectively) was not significantly affected by the pre-exercise meals (P>0.05). Total ATP utilisation (92.5±7.7, 94.8±5.3, 92.6±9.2 mol. min−1 for F, CHO and LCHO respectively) was also unaffected by the pre-exercise meals although there were significant changes in the rate of ATP use as a result of a change in exercise modality (p<0.01). Carbohydrate oxidation rate was significantly increased following CHO (p<0.01) and significantly reduced following LCHO meal (P>0.01). Conversely fat oxidation rate was suppressed (p<0.05) as a consequence of the availability of carbohydrate following CHO and increased following LCHO (p<0.01). CONCLUSIONS: Despite changes in substrate availability and differences in the oxidation rates of both carbohydrate and fat, duathlon performance and the rate at which ATP is utilised are not altered as a result of acute pre-exercise macronutrient manipulation.

The Answer to Weight Loss Is Easy—Doing It Is Hard!

IN BRIEF Although the number of people dieting continues to increase, the rate of obesity also continues to increase. The latest solution is the high-protein (or, more accurately, high-fat), low-carbohydrate diet. People lose weight while following this diet, but there is no evidence that the weight lost is maintained over the long term. In addition, the diet eliminates whole categories of foods known to have health benefits—fruits, whole-grains, vegetables, and milk. Energy restriction, not manipulation of macronutrients, is associated with weight reduction in the short term. Because we do not yet know how to maintain weight loss over the long-term, diabetes care providers should advise patients to eat healthfully, be physically active, and keep food and blood glucose records.

Regulation of galanin gene expression in the hypothalamic paraventricular nucleus of the obese Zucker rat by manipulation of dietary macronutrients

Lean and obese male Zucker rats were fed high fat (72% of energy as fat), high carbohydrate (66% of energy as carbohydrate) or intermediate diets for 4 weeks commencing 1 week after weaning. We examined the effects of these diets on growth rates, plasma insulin and corticosterone titres, and hypothalamic gene expression of 3 appetite-related neuropeptides. Messenger RNA levels for neuropeptide Y (NPY), galanin (GAL) and corticotropin-releasing factor (CRF) in critical hypothalamic locations were measured by in situ hybridization in each brain. Obese rats grew more rapidly and had elevated plasma insulin and corticosterone concentrations relative to their lean littermates. The obese phenotype was also associated with elevated NPY gene expression in the arcuate nucleus of the hypothalamus and increased GAL gene expression in the hypothalamic paraventricular nucleus. There was no effect of diet on NPY or CRF gene expression in either lean or obese rats. However, maintenance on the high fat diet had a significant effect on GAL gene expression in obese but not lean rats; high fat diet significantly reduced mRNA levels in the obese rats. This reduction in GAL mRNA was accompanied by attenuation of the hyperinsulinemia that is characteristic of this genetic obesity.

Special aspects of cancer prevention trials

The results of early cancer prevention trials now are being reported, and new trials have begun or are being designed. Initial trials used agents such as vitamins and minerals, generally regarded as safe. The trials in progress are using similar agents or macronutrient manipulation, but some have incorporated drugs with low but definite toxic potential, such as tamoxifen. Appropriate prevention trial design requires careful consideration of agent toxicity and the use of such agents in healthy individuals. Full disclosure of risks and benefits to potential subjects is necessary. Other considerations are study duration (usually very long) and subject number (usually very large), both of which increase the cost of a trial. Successful prevention trials must overcome these barriers through innovative design. Possible innovations include the use of intermediate marker end-points, the enrollment of subjects at high risk for a specific cancer, and the use of volunteers to help conduct trials.