Nutrients2014, 6(10), 4625-4639; doi:10.3390/nu6104625 - published 22 October 2014 Show/Hide Abstract
Abstract: The aim of the present study was to evaluate the potential association between dietary nutrients and alterations in DNA methylation in a set of five candidate genes, including CD14, Et-1, iNOS, HERV-w and TNFα, in a population of overweight/obese subjects. We evaluated possible associations between gene methylation and clinical blood parameters, including total cholesterol (TC), low- and high-density lipoprotein cholesterol (LDL-C and HDL-C), triglyceride and homocysteine levels. We employed validated methods to assess anthropometric, clinical and dietary data, as well as pyrosequencing to evaluate DNA methylation of the five candidate genes in 165 overweight/obese subjects. There was no association between body mass index and DNA methylation of the five candidate genes in this group of subjects. Positive associations were observed between TNFα methylation and blood levels of LDL-C (β = 0.447, p = 0.002), TC/HDL-C (β = 0.467, p = 0.001) and LDL-C/HDL-C (β = 0.445, p = 0.002), as well as between HERV-w methylation and dietary intakes of β-carotene (β = 0.088, p = 0.051) and carotenoids (β = 0.083, p = 0.029). TNFα methylation showed negative associations with dietary intakes of cholesterol (β = −0.278, p = 0.048), folic acid (β = −0.339, p = 0.012), β-carotene (β = −0.332, p = 0.045), carotenoids (β = −0.331, p = 0.015) and retinol (β = −0.360, p = 0.008). These results suggest a complex relationship among nutrient intake, oxidative stress and DNA methylation.
Nutrients2014, 6(10), 4610-4624; doi:10.3390/nu6104610 - published 22 October 2014 Show/Hide Abstract
Abstract: The effects of fermented paste made from soybean, brown rice, or brown rice in combination with rice bran or red ginseng marc on the glucose metabolism and antioxidative defense system in high fat-fed mice were investigated. The mice were given experimental diets for eight weeks: Normal control, high fat, and high fat supplemented with soybean fermented paste, brown rice fermented paste, brown rice-rice bran fermented paste, or brown rice-red ginseng marc fermented paste. The high fat group showed markedly higher blood glucose level and erythrocyte lipid peroxidation than the normal control group. Diet supplementation of fermented paste inhibited the high fat-induced hyperglycemia and oxidative stress via regulation of the glucose-regulating and antioxidant enzymes activities. The soybean and brown rice-red ginseng marc fermented pastes were the most effective in improving the glucose metabolism and antioxidant defense status in mice under high fat diet condition. These findings illustrate that brown rice, in combination with red ginseng marc, may be useful in the development of fermented paste with strong hypoglycemic and antioxidative activities.
Nutrients2014, 6(10), 4591-4609; doi:10.3390/nu6104591 - published 22 October 2014 Show/Hide Abstract
Abstract: Eating disorders are multifactorial conditions that can involve a combination of genetic, metabolic, environmental, and behavioral factors. Studies in humans and laboratory animals show that eating can also be regulated by factors unrelated to metabolic control. Several studies suggest a link between stress, access to highly palatable food, and eating disorders. Eating “comfort foods” in response to a negative emotional state, for example, suggests that some individuals overeat to self-medicate. Clinical data suggest that some individuals may develop addiction-like behaviors from consuming palatable foods. Based on this observation, “food addiction” has emerged as an area of intense scientific research. A growing body of evidence suggests that some aspects of food addiction, such as compulsive eating behavior, can be modeled in animals. Moreover, several areas of the brain, including various neurotransmitter systems, are involved in the reinforcement effects of both food and drugs, suggesting that natural and pharmacological stimuli activate similar neural systems. In addition, several recent studies have identified a putative connection between neural circuits activated in the seeking and intake of both palatable food and drugs. The development of well-characterized animal models will increase our understanding of the etiological factors of food addiction and will help identify the neural substrates involved in eating disorders such as compulsive overeating. Such models will facilitate the development and validation of targeted pharmacological therapies.
Nutrients2014, 6(10), 4552-4590; doi:10.3390/nu6104552 - published 21 October 2014 Show/Hide Abstract
Abstract: Obesity is a global issue and it has been suggested that an addiction to certain foods could be a factor contributing to overeating and subsequent obesity. Only one tool, the Yale Food Addiction Scale (YFAS) has been developed to specifically assess food addiction. This review aimed to determine the prevalence of food addiction diagnosis and symptom scores, as assessed by the YFAS. Published studies to July 2014 were included if they reported the YFAS diagnosis or symptom score and were published in the English language. Twenty-five studies were identified including a total of 196,211 predominantly female, overweight/obese participants (60%). Using meta-analysis, the weighted mean prevalence of YFAS food addiction diagnosis was 19.9%. Food addiction (FA) diagnosis was found to be higher in adults aged >35 years, females, and overweight/obese participants. Additionally, YFAS diagnosis and symptom score was higher in clinical samples compared to non-clinical counterparts. YFAS outcomes were related to a range of other eating behavior measures and anthropometrics. Further research is required to explore YFAS outcomes across a broader spectrum of ages, other types of eating disorders and in conjunction with weight loss interventions to confirm the efficacy of the tool to assess for the presence of FA.
Nutrients2014, 6(10), 4531-4551; doi:10.3390/nu6104531 - published 21 October 2014 Show/Hide Abstract
Abstract: Body weight stability may imply active regulation towards a certain physiological condition, a body weight setpoint. This interpretation is ill at odds with the world-wide increase in overweight and obesity. Until now, a body weight setpoint has remained elusive and the setpoint theory did not provide practical clues for body weight reduction interventions. For this an alternative theoretical model is necessary, which is available as the settling point model. The settling point model postulates that there is little active regulation towards a predefined body weight, but that body weight settles based on the resultant of a number of contributors, represented by the individual’s genetic predisposition, in interaction with environmental and socioeconomic factors, such as diet and lifestyle. This review refines the settling point model and argues that by taking body weight regulation from a settling point perspective, the road will be opened to careful dissection of the various contributors to establishment of body weight and its regulation. This is both necessary and useful. Nutrigenomic technologies may help to delineate contributors to body weight settling. Understanding how and to which extent the different contributors influence body weight will allow the design of weight loss and weight maintenance interventions, which hopefully are more successful than those that are currently available.
Nutrients2014, 6(10), 4520-4530; doi:10.3390/nu6104520 - published 21 October 2014 Show/Hide Abstract
Abstract: We compared the effects of oral administration of high-dose or low-dose glutamine dipeptide (GDP), alanine (ALA), glutamine (GLN), and ALA + GLN on the blood availability of amino acids in rats submitted to insulin-induced hypoglycemia (IIH). Insulin detemir (1 U/kg) was intraperitoneally injected to produce IIH; this was followed by oral administration of GDP, GLN + ALA, GLN, or ALA. We observed higher blood levels of GLN, 30 min after oral administration of high-dose GDP (1000 mg/kg) than after administration of ALA (381 mg/kg) + GLN (619 mg/kg), GLN (619 mg/kg), or ALA (381 mg/kg). However, we did not observe the same differences after oral administration of low-dose GDP (100 mg/kg) compared with ALA (38.1 mg/kg) + GLN (61.9 mg/kg), GLN (61.9 mg/kg), or ALA (38.1 mg/kg). We also observed less liver catabolism of GDP compared to ALA and GLN. In conclusion, high-dose GDP promoted higher blood levels of GLN than oral ALA + GLN, GLN, or ALA. Moreover, the lower levels of liver catabolism of GDP, compared to ALA or GLN, contributed to the superior performance of high-dose GDP in terms of blood availability of GLN.