Soy-dairy protein blend and whey protein ingestion after resistance exercise increases amino acid transport and transporter expression in human skeletal muscle.

Increasing amino acid availability (via infusion or ingestion) at rest or postexercise enhances amino acid transport into human skeletal muscle. It is unknown whether alterations in amino acid availability, from ingesting different dietary proteins, can enhance amino acid transport rates and amino acid transporter (AAT) mRNA expression. We hypothesized that the prolonged hyperaminoacidemia from ingesting a blend of proteins with different digestion rates postexercise would enhance amino acid transport into muscle and AAT expression compared with the ingestion of a rapidly digested protein. In a double-blind, randomized clinical trial, we studied 16 young adults at rest and after acute resistance exercise coupled with postexercise (1 h) ingestion of either a (soy-dairy) protein blend or whey protein. Phenylalanine net balance and transport rate into skeletal muscle were measured using stable isotopic methods in combination with femoral arteriovenous blood sampling and muscle biopsies obtained at rest and 3 and 5 h postexercise. Phenylalanine transport into muscle and mRNA expression of select AATs [system L amino acid transporter 1/solute-linked carrier (SLC) 7A5, CD98/SLC3A2, system A amino acid transporter 2/SLC38A2, proton-assisted amino acid transporter 1/SLC36A1, cationic amino acid transporter 1/SLC7A1] increased to a similar extent in both groups (P < 0.05). However, the ingestion of the protein blend resulted in a prolonged and positive net phenylalanine balance during postexercise recovery compared with whey protein (P < 0.05). Postexercise myofibrillar protein synthesis increased similarly between groups. We conclude that, while both protein sources enhanced postexercise AAT expression, transport into muscle, and myofibrillar protein synthesis, postexercise ingestion of a protein blend results in a slightly prolonged net amino acid balance across the leg compared with whey protein.

White hat bias: examples of its presence in obesity research and a call for renewed commitment to faithfulness in research reporting.

'White hat bias' (WHB) (bias leading to distortion of information in the service of what may be perceived to be righteous ends) is documented through quantitative data and anecdotal evidence from the research record regarding the postulated predisposing and protective effects of nutritively sweetened beverages and breastfeeding, respectively, on obesity. Evidence of an apparent WHB is found in a degree sufficient to mislead readers. WHB bias may be conjectured to be fuelled by feelings of righteous zeal, indignation toward certain aspects of industry or other factors. Readers should beware of WHB, and our field should seek methods to minimize it.

Critical review of the World Health Organization's (WHO) 2007 report on 'evidence of the long-term effects of breastfeeding: systematic reviews and meta-analysis' with respect to obesity.

Obesity among children and adults has become a highly recognized public health concern and there is an increasing need to discover causes and evaluate preventative measures. One putatively causal influence on obesity is breastfeeding (BF). The World Health Organization (WHO) recently published a report (WR) on 'Evidence of the Long-Term Effects of Breastfeeding: Systematic Reviews and Meta-Analysis' and concluded 'that the evidence suggests that breastfeeding may have a small protective effect[emphasis added] on the prevalence of obesity . . . [and] the effect of breastfeeding was not likely to be due to publication bias or confounding.' Here we provide a critical overview of the WR's section on BF and obesity by addressing eight questions: Q1: Is there sufficient evidence to conclude that BF is associated with lower rates of obesity in children? Q2: Is there sufficient evidence to conclude that BF is associated with lower rates of obesity among breastfed offspring once they reach adulthood? Q3: If there are such associations, what are their magnitudes in comparison with other putatively causal factors and with respect to the potential impact on individual or population levels of obesity? Q4: Is there sufficient evidence to conclude that BF causes a reduction in risk of obesity during childhood? Q5: Is there sufficient evidence to conclude that BF does not cause a reduction in risk of obesity during childhood? Q6: Is there sufficient evidence to conclude that BF causes a long-term reduction in risk of obesity that persists into adulthood? Q7: Is there sufficient evidence to conclude that BF does not cause a long-term reduction in risk of obesity that persists into adulthood? Q8: What further research might be done to address these questions? We conclude that, while BF may have benefits beyond any putative protection against obesity, and benefits of BF most likely outweigh any harms, any statement that a strong, clear or consistent body of evidence shows that BF causally reduces the risk of overweight or obesity is unwarranted at this time.

The potential role of soyfoods in weight and adiposity reduction: an evidence-based review.

Evidence concerning the relationship between soyfoods and weight loss was reviewed. Detailed searches of PubMed and Web of Science were performed to identify and evaluate evidence for or against four propositions related to soyfoods and weight loss (Data from in vitro, animal, epidemiologic, and clinical studies were evaluated and summarized). (1) Certain soyfoods will improve weight and/or fat loss when fed at isolcaloric levels (similar calories given across experimental conditions, but not necessarily at a level to maintain current body weight); generally supportive evidence in animal studies, but there is no compelling support in human studies. (2) Certain soyfoods will improve weight and fat loss when included as part of a diet by affecting caloric intake; limited supportive evidence in animal and human studies. (3) Certain soyfoods will prevent/improve risk factors related to glucoregulatory function and cardiovascular health during weight loss; some evidence supporting this proposition, but additional evidence is needed before conclusions can be made. (4) Certain soyfoods will minimize the loss of bone mass during weight loss; no data available pertinent to this proposition. Limitations in existing data make it difficult to reach conclusions regarding these four propositions. Overall, the current data suggest that soyfoods are as good as other protein sources for promoting weight loss and there is a suggestive body of evidence that soyfoods may confer additional benefits, but results must be carefully interpreted and additional evidence is needed before making firm conclusions concerning soyfoods and weight loss.

No effect of dietary fat on short-term weight gain in mice treated with atypical antipsychotic drugs.

RATIONALE: Atypical antipsychotic drugs (AAD) induce significant weight gain in female C57BL/6J mice. The effect of dietary fat on weight gain and serum lipids in this model is unknown. OBJECTIVES: Test the hypothesis that the obesigenic effects of these drugs are greater in the presence of a high-fat diet. METHODS: Female C57BL/6J mice were treated with atypical antipsychotics for 3 weeks and fed either a low-fat or high-fat diet (4.6 vs 15.6% fat by wt). Food intake (FI), body weight (BW), body composition, and serum lipids were measured during treatment with optimized doses of olanzapine, quetiapine, and risperidone. Energy intake (EI) and feed efficiency (FE) were calculated. Group differences in change were analyzed via repeated measures analysis of variance (ANOVA). Serum lipid concentrations, EI and FE were compared using two-way ANOVA. RESULTS: AAD-treated mice gained significantly more weight than controls after 3 weeks (P<0.001). Treatment and diet had significant effects on FI and EI over time (P<0.001). AAD-treated mice had significantly higher FE than controls (P<0.05); however, there was no significant drug by diet interaction (P=0.65). Risperidone low-fat mice gained significantly more absolute fat mass than placebo low-fat mice (P<0.05). All treatment groups, except quetiapine low-fat and olanzapine high-fat, gained significantly more absolute lean mass than placebo controls (P<0.05). Cholesterol levels were significantly lower in quetiapine and risperidone than placebo (P<0.05). Risperidone low-fat mice had significantly higher triglyceride levels than placebo and risperidone high-fat mice (P<0.05). CONCLUSIONS: A high-fat diet does not increase AAD-induced BW gain in female mice during a 3-week treatment period.

Antipsychotic drug-induced weight gain: development of an animal model.

OBJECTIVE: Weight gain is a prominent effect of most atypical antipsychotic drugs (AAPDs); yet, the mechanisms are not fully understood and no well-established mouse models exist for investigating the mechanisms. Thus, we developed a mouse model to evaluate the effects of AAPDs on eating, body weight (BW), and body composition. METHODS: Female C57BL/6J mice were used to test olanzapine, quetiapine, ziprasidone, and risperidone. Mice were acclimated to individual housing, given ad libitum access to chow and water, dosed with placebo peanut butter pills for 1 week, and then dosed daily with AAPD-laced peanut butter pills for 4 weeks. Weekly food intakes and BWs were measured, and body compositions were determined at the end of each experiment. RESULTS: After 4 weeks of treatment, olanzapine, quetiapine, ziprasidone, and risperidone caused significant weight increases, but only olanzapine and quetiapine were associated with significantly increased food intake. Body composition data revealed that olanzapine-treated mice had more relative fat mass and risperidone-treated mice had more relative lean mass than did control mice. Quetiapine and ziprasidone did not significantly affect relative body composition even though BW was increased. CONCLUSIONS: Oral AAPD administration causes increased BW in female mice. Our mouse model of AAPD-induced weight gain resembles the human response to these medications and will be used to investigate the mechanisms for weight gain and fat accumulation.

Effect of high retinoid doses on RAR-beta mRNA expression in female B6D2F1 mice.

The expression of retinoid receptors is altered during the development of several types of cancer. In the present study, we determined the influence of high dietary concentrations of 4-hydroxyphenylretinamide (4-HPR) and 13-cis-retinoic acid (13-cis-RA) on RAR-beta mRNA expression in female mice. Expression of liver and lung RAR-beta RNA increased with increasing levels of dietary retinoid (both 4-HPR and 13-cis RA). Bladder RAR-beta mRNA levels, however, were significantly decreased in mice fed 13-cis RA or 4-HPR. These results suggest that feeding high levels of retinoids to mice results in tissue-specific elfects on expression of RAR-beta mRNA.