It has been more than three decades since the first assay assessing circulating 25 (OH)D in human subjects was performed That publication as well as several that followed it defined 'normal' nutritional vitamin D status in human populations. Recently, the wisdom by which 'normal' circulating 25 (OH)D levels in human subjects were assigned in the past has come under question. It appears that sampling human subjects, who appear to be free from disease, and assessing 'normal' circulating 25 (OH)D levels by plotting a Gaussian distribution is grossly inaccurate. There are many reasons why this method is inaccurate, including race, lifestyle habits, sunscreen usage, age, latitude, and inappropriately low dietary recommendations for vitamin D. For instance, a 400 IU/day. AI for vitamin D is insignificant when one considers that a 10-15 minute whole body exposure to peak summer sun will generate and release up to 20,000 IU vitamin $D_3$ into the circulation. Recent studies, which orally administered up to 10,000 IU/day vitamin $D_3$ to human subjects for several months, have successfully elevated circulating 25 (OH)D levels to those observed in individuals from sun-rich environments. Further, we are now able to accurately assess sufficient circulating 25 (OH)D levels utilizing specific biomarkers instead of guessing what an adequate level is. These biomarkers include intact parathyroid hormone (PTH), calcium absorption, bone mineral density (BMD), insulin resistance and pancreatic beta cell function. Using the data from these biomarkers, vitamin D deficiency should be defined as circulating levels of 25 (OH)D$\leq$30 ng/mL. In certain cases, such as pregnancy and lactation, significantly higher circulating 25 (OH)D levels would almost certainly be beneficial to both the mother and recipient fetus/infant.
As obesity is known to be related to hyperlipidemia, insulin and leptin resistance, and other chronic diseases, much recent research has focused on functional food materials and their anti-obesity activity. This study was performed to study the effects of Artemisia Iwayomogi oligosaccharide AIPI on the anti-obesity function in normal rats and diet-induced obese (DIO) rats. F344 male rats were divided into four groups: Normal-control (CONT), normal-AIPI, DIO-CONT and DIO-AIPI. The groups were provided with water (in the CONT groups) or another drink for 4 weeks. The final body weights of rats in the DIO-AIPI group were lower than those in the CONT group. Abdominal adipose tissue weight per kg of body weight in the DIO-AIPI group was significantly lower than that in the DIO-CONT group. Also, the final levels of serum-triglyceride, serum-total cholesterol and serum-low density lipoprotein cholesterol in the DIO-AIPI group were lower than those in the DIO-CONT group. Moreover, the serum-high density lipoprotein cholesterol level in the normal-AIPI group was significantly higher than that in the normal-CONT group. Finally, the serum-leptin concentration was significantly lower in the DIO-AIPI group. Total lipid, triglyceride, and total cholesterol contents in the feces of the DIO-AIPI group were as high as 142%, 199%, and 165% of the respective values of the DIO-CONT GROUP. These results indicate that orally administered Artemisia Iwayomogi oligosaccharide not only has hypotriglycemic and hypocholesterolemic effects, but also has the effect of reducing the body weight and the abdominal adipose tissue weights obese rats. Therefore, we expect that Artemisia Iwayomogi oligosaccharide AIPI may have an anti-obesity function in F344 diet-induced obese rats. (Korean J Nutrition 36(5): 437∼445, 2003)
Complex microbial communities play an important role in the human health and co-evolved with human in the form of symbiosis. Many literatures provide new evidences that the increased prevalence of obesity cannot be attributed solely to changes in the human genome, nutritional habits, or reduction of physical activity in our daily lives. The intestinal flora was recently proposed as an environmental factor responsible for the control of body weight and energy metabolism. A number of studies suggest that the modulation of gut microbiota affects host metabolism and has an impact on energy storage and demonstrated a role for the gut microbiota in weight gain, fat increase, and insulin resistance. Variations in microbiota composition are found in obese humans and mice and the microbiota from an obese mouse confers an obese phenotype when transferred to an axenic mouse. As well, the gut microbial flora plays a role in converting nutrients into calories. Specific strategies for modifying gut microbiota may be a useful means to treat or prevent obesity. Dietary modulations of gut microbiota with a view to increasing bifidobacteria have demonstrated to reduce endotoxemia and improve metabolic diseases such as obesity. The fermentation of medicinal herbs is intended to exert a favorable influence on digestability, bioavailability and pharmacological activity of herbal extract. Therefore we also expect that the fermented herbal extracts may open up a new area to treat obesity through modulating gut microbiota.
The purpose of this study was to analyze the relationships among zinc status, protein and phytate intake, and diabetic control indices of type 2 diabetic women. The mean age and the duration of diabetes were respectively 57.9±6.9 years old and 8.0±6.5 years. The mean daily energy intake of diabetic subjects was 1562 kcal. Both the zinc intake (6.2mg/day) and the zinc %RI (% of The Recommended Intake for zinc: 79.5%) of the diabetic participants were significantly lower than those of the control group (respectively p<0.01). As for the diabetic group, the higher the energy intake (kcal/day), the higher were the zinc intake (p<0.001) and %RI for zinc (p<0.001). Zinc intake was positively correlated with the protein (p<0.001), animal protein (p<0.001), and fat intake (p<0.001), but negatively correlated with the carbohydrate intake (p<0.001). Foods with high amount of phytate were the major source of zinc (p<0.01), but did not contribute to high zinc densities. The urinary zinc excretion was twice as high as in the diabetic group compared to the control group (p<0.001). In addition, the urinary zinc loss was positively correlated with the duration of diabetes (p<0.05), hyperglycemia (p<0.001) and insulin resistance (p<0.05). %RI for zinc was negatively correlated with the HbA1C (p<0.05). These results lead us to conclude that the appropriate intake of energy controlled by diet therapy could improve the total zinc intake and %RI for zinc in diabetic women. Also, normal blood glucose level controlled by diet therapy could improve the hyperzincuria. Dietetic practitioners should encourage consumption patterns that provide zinc-rich foods in the form of animal protein to improve the bioavailability as well as the total daily intake of zinc.
The effects of cardiac ischemia-reperfusion and $\beta$-adrenergic stimulation on metabolic function and energetics were investigated in Lan gendorff-perfused spontaneously hypertensive rat (SHR) hearts. Sarcoplasmic reticulum {TEX}$Ca^{2+}${/TEX}-dependent ATPase and cardiac lactate dehydrogenase (LDH) are additionally studied. The perfusion medium (1.0 mM {TEX}$Ca^{2+}${/TEX}) contained 5 mM glucose(+5 U/L insulin) and 2 mM pyruvate as substrates. Global ischemia was induced by reducing perfusion pressure of 100 to 40 cm {TEX}$H_{2}${/TEX}O, followed by 20 min reperfusin. Isoproterenol (ISO, 1$\mu$M) was infused for 10 min. Coronary vascular resistance and myocardial oxygen consumption ({TEX}$MVO_{2}${/TEX}) of SHR were increased in parallel with enhanced venous lactate during ischemia and reperfusion compared to those of Sprague Dawley (SD) hearts. Although ischemia-induced increase in venous lactate and combined adenosine plus inosine was abolished, coronary vasodilation produced in SD during reperfusion. In SHR, depressed reactive hyperemia was associated with a fall in cardiac ATP and CrP/Pi ratio and a rise in intracellular lactate/Pyruvate ratio. On the other hand, ISO produced coronary functional hyperemia and an increase in {TEX}$MVO_{2}${/TEX}. However, these responses were less than those in SHR hearts. The ATPase activity of SHR was attenuated in free {TEX}$Ca^{2+}${/TEX} concentrations used under basal condition and with ISO compared to that of SD. Venous lactate output and cardiac LDH activity were augmented in SHR as influenced by ISO. These results demonstrate that coronary reactive and functional hyperemia was dpressed in SHR, which cold be explained by alterations in the cytosolic phosphorylation potential and the cytosolic redox state manipulated by LDH, and by abnormal free calcium handling.
Chronic inflammation has been implicated as one of the important etiological factors in insulin resistance and type 2 diabetes mellitus (T2DM). To investigate the role of anti-inflammatory cytokines in the development of T2DM, we conducted a case-control study to assess the association between IL4/IL4R polymorphisms and disease risk. We firstly identified single nucleotide poly-morphisms (SNP) at IL4 and IL4RA loci by sequencing the loci in Korean participants. Case-control studies were conducted by genotyping the SNPs in 474 T2DM cases and 470 non-diabetic controls recruited from community-based cohorts. Replication of the associated signals was performed in 1,216 cases and 1,352 controls. We assessed effect of IL4 -IL4RA interaction on T2DM using logistic regression method. The functional relevance of the SNP associated with disease risk was determined using a reporter expression assay. We identified a strong association between the IL4 promoter variant rs2243250 and T2DM risk (OR=0.77; 95% CI, 0.67~0.88; p=$1.65{\times}10^{-4}$ in the meta-analysis). The reporter gene expression assay demonstrated that the presence of rs2243250 might affect the gene expression level with ~1.5-fold allele difference. Our findings contribute to the identification of IL4 as a T2D susceptibility locus, further supporting the role of anti-inflammatory cytokines in T2DM disease development.
Purpose: Recent studies have suggested that decreased serum potassium level may contribute to various metabolic disorders in adult patients including nonalcoholic fatty liver disease (NAFLD). We aimed to study the correlation between serum potassium levels and the histologic severity of NAFLD in children. Methods: Pediatric patients with biopsy-proven NAFLD were included in this study. Demographic, clinical, and histopathological data were obtained. Multivariable logistic regression analysis was used to assess whether potassium levels are associated with the presence of nonalcoholic steatohepatitis (NASH) or fibrosis after adjusting for possible confounders. A p-value <0.05 was considered statistically significant. Results: Among 125 biopsies, 49.6% (62) had evidence of NASH while 66.4% (83) had some degree of fibrosis (stage 1-3). Mean serum potassium was significantly lower in NASH group as compared to non-NASH group ($4.4{\pm}0.42mmoL/L$ vs. $4.8{\pm}0.21$, p<0.001). Higher potassium level had negative correlation with presence of steatosis, ballooning, lobular inflammation, fibrosis and NAFLD activity score (p<0.05). On multivariable analysis and after adjusting for the metabolic syndrome and insulin resistance, higher potassium level was significantly associated with lower likelihood of having a histological diagnosis of NASH on biopsy (odds ratio [OR], 0.12; 95% confidence interval [95% CI], 0.05-0.28; p<0.001). Similarly, the likelihood of having fibrosis decreases by 76% for every 0.5 mmoL/L increase in potassium (OR, 0.24; 95% CI, 0.11-0.54; p<0.001). Conclusion: Our study shows an inverse relationship between serum potassium levels and the presence of aggressive disease (NASH and fibrosis) in children with NAFLD.
Objective: This study was performed to investigate the prevalence of impaired fasting glucose (IFG) and its related characteristics among healthy adults in some Korean rural areas. Methods: We conducted a cross-sectional study using the data from 1352 adults who were over the age 40 and under the age 70 and who were free of diabetes mellitus (DM), cardiovascular diseases and other diseases and who participated in a survey conducted as part of the Korean Rural Genomic Cohort Study. IFG was defined as a serum fasting glucose level between 100 and 125 mg/dL. Results: The prevalence of IFG was 20.4% in men, 15.5% in women and 12.7% overall. Multivariate logistic regression analysis demonstrated that the independent risk factors for IFG were male gender, having a family history of DM, the quartiles of gamma glutamyltransferase and high sensitive C-reactive protein and the waist circumference. The homeostatis model assessment for insulin resistance was very strongly associated with IFG. The prevalence of metabolic syndrome (MS) and MS components was higher in the subjects with IFG then in those with normal fasting glucose (NFG). Conclusions: The result of study could supply evidence to find the high risk population and to determine a strategy for treating IFG. Further research is needed to explain the causal relationship and mechanisms of IFG.
Porcine colostrum and milk were separated into the acid-soluble and casein fractions by acidification followed by centrifuge. The acid-soluble fraction of porcine colostrum was further separated by liquid chromatography and anisotropic membrane filtration. Trypsin and chymotrypsin inhibitory capacity in porcine colostrum, milk and their components was determined by incubating bovine trypsin or chymotrypsin in a medium containing their corresponding substrates with or without addition of various amounts of porcine colostrum, porcine milk or their components. The inhibition of insulin-like growth factor I (IGF-I) and epidermal growth factor (EGF) degradation in pig small intestinal contents by porcine colostrum was measured by incubating iodinated IGF-I or EGF with the intestinal contents with or without addition of porcine colostrum. Degradation of labeled IGF-I or EGF was determined by monitoring the generation of radioactivity soluble in 30% trichloroacetic acid (TCA). The results showed that porcine colostrum had high levels of trypsin and chymotrypsin inhibitory activity and increased the stability of IGF-I and EGF in pig intestinal contents. The inhibitory activity declined rapidly during lactation. It was also found that trypsin and chymotrypsin inhibitory activity and the inhibition on IGF-I and EGF degradation in the acid-soluble fraction were higher than that in the casein fraction. Heat-resistance study indicated that trypsin inhibitors in porcine colostrum survived heat treatments of $100^{\circ}C$ water bath for up to 10 min, but exposure to boiling water bath for 30 min significantly decreased the inhibitory activity. Compared with the trypsin inhibitors, the chymotrypsin inhibitors were more heatsensitive. Separation of the acid-soluble fraction of porcine colostrum by liquid chromatography and anisotropic membrane filtration revealed that the trypsin and chymotrypsin inhibitory capacity was mainly due to a group of small proteins with molecular weight of 10,000-50,000. In conclusion, the present study confirmed the existence of high levels of protease inhibitors in porcine colostrum, and the inhibition of porcine colostrum on degradation of milk-borne growth factors in the pig small intestinal tract was demonstrated for the first time.
Scientific evidence for the primary prevention of cancer caused by physical activity of regular moderate-intensity or greater is rapidly accumulating in this field. About 300 epidemiologic studies on the association between physical activity and cancer risk have been conducted worldwide. The objectives of this paper were three-fold: (i) to describe briefly the components of physical activity and its quantification; (ii) to summarize the most important conclusions available from comprehensive reports, and reviews of the epidemiologic individual and intervention studies on a role physical activity in cancer prevention; (iii) to present proposed biological mechanisms accounting for effects of activity on cancer risk. The evidence of causal linked physical activity and cancer risk is found to be strong for colon cancer - convincing; weaker for postmenopausal breast and endometrium cancers - probable; and limited suggestive for premenopausal breast, lung, prostate, ovary, gastric and pancreatic cancers. The average risk reductions were reported to be 20-30%. The protective effects of physical activity on cancer risk are hypothesized to be through multiple interrelated pathways: decrease in adiposity, decrease in sexual and metabolic hormones, changes in biomarkers and insulin resistance, improvement of immune function, and reduction of inflammation. As there are several gaps in the literature for associations between activity and cancer risk, additional studies are needed. Future research should include studies dealing with limitations in precise estimates of physical activity and of a lack of consensus on what defines sedentary behavior of individuals and those linked with the proposed biomarkers to cancer risk and controlled exercise intervention trials.
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