BackgroundLactobacillus gasseri BNR17 is a type of probiotic strain isolated from human breast milk. A study was reported regarding the fact that BNR17 was an inhibitor of obesity and diabetic activities in the human body through previous animal experiments. This study was furthered to investigate the effect of BNR17, a probiotic strain isolated from human breast milk, on obese and overweight adults.MethodsSixty-two obese volunteers aged 19 to 60 with body mass index ≥ 23 kg/m2 and fasting blood sugar ≥ 100 mg/dL participated in a placebo controlled, randomized, and double-blind trial. For 12 weeks, 57 participants were given either placebo or BNR17 and were tested by measuring body fat, body weight, various biochemical parameters, vital signs, and computed tomography at the start of the study and at weeks 4, 8, and 12. The subjects assumed usual daily activities without having to make behavioral or dietary modifications during the course of the study.ResultsAt the 12th week, a slight reduction in body weight was noted in the BNR17 group, but there were no significant weight changes between groups. Decrease of waist and hip circumferences in the BNR17 group was more pronounced than those in the placebo group. The two groups had no special or severe adverse reactions.ConclusionDespite there being no change in behavior or diet, administration of only the supplement of BNR17 reduced weight and waist and hip circumference. However, there were no significant differences between the two groups. These findings warrant a subsequent longer-term prospective clinical investigation with a large population.

This study demonstrated that self-reported height and weight may lead to the underestimation of BMI and consequently the prevalence of obesity. These biases should be taken into account when self-reported data are used for monitoring the prevalence and trends of obesity among adolescents nationwide.

This study demonstrated that the reliability estimates for the KYRBWS questionnaire are varied, but generally reliable over time. The indices with low reliability estimates need to be evaluated further in order to determine whether the indices should be modified or deleted from future versions of the KYRBWS.

ObjectivesThis study was conducted to observe recent changes in adolescents' dietary behavior and indirectly evaluate the effects of the government's nutritional policies in Korea.MethodsWe analyzed the secular trends in seven dietary behaviors using the Korea Youth Risk Behavior Web-based Survey data from 2005 to 2009. Through literature review, we included the policies implemented for the improvement of adolescents'dietary behaviors during the same periods.ResultsThe significant linear trends were observed in all dietary behaviors (p<0.05). Overall, all behaviors except the fruit intake rate were desirably changed during five years but undesirable changes were observed between 2008 and 2009 in all behaviors. Within those periods, several policies were implemented including 'Ban on carbonated-beverages in school', 'Green Food Zone', etc. Despite confirmed evidence of their effects, the policies on individual behavior such as nutrition education didn't influence the prevalence of dietary behaviors because they were conducted to too limited persons. Polices on the school environmental improvement, such as ban on carbonated beverage in school, were more effective because they decreased the exposure of undesirable food environment. However, for effect of Green Food Zone improving community environment we couldn't come to a conclusion because of too short period after full implementation.ConclusionsAmong government nutrition policies conducted from 2005 to 2009, those on environmental improvement, especially in school, were more effective than those on individual behavior. Therefore, the development and implement of policies on school environmental improvement are needed in Korea.

AMP-activated protein kinase (AMPK) acts as a cellular energy sensor, being activated during states of low energy charge. Hypothalamic AMPK activity is altered by hormonal and metabolic signals and mediates the feeding response. To determine the effect of diabetes on hypothalamic AMPK activity, we assayed this activity in streptozotocin (STZ)-induced diabetic rats. Compared with control rats, STZ-induced diabetic rats had significant hyperphagia and weight loss. Hypothalamic AMPK phosphorylation and ␣2-AMPK activity were higher and acetyl-CoA carboxylase activity was lower in diabetic rats than in control rats. Chronic insulin treatment or suppression of hypothalamic AMPK activity completely prevented diabetesinduced changes in food intake as well as in hypothalamic AMPK activity and mRNA expression of neuropeptide Y and proopiomelanocortin. Plasma leptin and insulin levels were profoundly decreased in diabetic rats. Intracerebroventricular administration of leptin and insulin reduced hyperphagia and the enhanced hypothalamic AMPK activity in diabetic rats. These data suggest that leptin and insulin deficiencies in diabetes lead to increased hypothalamic AMPK activity, which contributes to the development of diabetic hyperphagia. Diabetes 54:63-68, 2005 D iabetes is characterized by altered fuel metabolism due to relative or absolute deficiency of insulin. Individuals with uncontrolled diabetes commonly experience hyperphagia (1), which makes glycemic control more difficult. Several mechanisms of diabetic hyperphagia have been suggested. For example, the expression of hypothalamic orexigenic neuropeptides, neuropeptides Y (NPY) and agouti-related protein (AgRP), is increased in diabetic animals, while expression of anorexigenic proopiomelanocortin (POMC) and corticotropin-releasing peptide (CRH) is decreased (2-4). Plasma levels of leptin and insulin are decreased in streptozotocin (STZ)-induced diabetic rats, and administration of insulin and leptin prevents diabetic hyperphagia and normalizes the levels of hypothalamic neuropeptides (5-8). These findings suggest that in diabetic animals, a deficiency of two hormones, insulin and leptin, causes hyperphagia by altering the balance of hypothalamic neuropeptides, but the intraneuronal signaling mechanisms causing diabetic hyperphagia are still incompletely understood.AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase that is activated when cellular energy is depleted (9,10). Once activated, the enzyme reduces the activities of ATP-consuming anabolic pathways and increases the activities of energy-producing catabolic pathways, acting to reestablish normal cellular energy balance.AMPK is also expressed in the hypothalamic neurons involved in the regulation of food intake (11). Recent studies by our group and others have demonstrated the importance of hypothalamic AMPK in regulating food intake (12)(13)(14). Food intake and body weight were increased by overexpression of the constitutively active AMPK gene but were decreased by overexpression of...