Journal of the Korean Society of Food Science and Nutrition
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v.43
no.5
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pp.763-771
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2014
The objective of this study was to assess the relationship between dietary sodium intake and prevalence of abdominal obesity in Korean adults. We used data from the Korea National Health and Nutrition Examination Survey V-1 and analyzed data on 4,475 Koreans (${\geq}30$ years old). Subjects were divided into three groups according to fasting plasma glucose (FPG): 1) normal (FPG <100 mg/dL), 2) pre-diabetes ($100mg/dL{\leq}FPG{\leq}125mg/dL$), and 3) diabetes (FPG ${\geq}126mg/dL$ or subjects diagnosed with diabetes). The subjects in each category were stratified by dietary sodium intake as well as index of abdominal obesity. We found that dietary sodium intake was positively correlated with waist circumference (WC) (P=0.002) and was particularly high in the pre-diabetes group. In multiple logistic regression analysis, the normal and diabetes groups showed no association between dietary sodium intake and WC, whereas the pre-diabetes group with a high sodium intake exhibited a significant association (odds ratio (OR)=1.479, P=0.029) between dietary sodium intake and WC. Further, the OR for abdominal obesity in the high sodium intake group with pre-diabetes was 1.590 after adjusting for age and sex (P=0.012). In addition, the ORs for the prevalence of abdominal obesity with fasting glucose, fasting insulin, and homeostasis model assessment of insulin resistance were significantly higher in the pre-diabetes group with high sodium intake compared with low sodium intake. Moreover, these associations were significant even after adjusting for confounding variables (model 2: age and sex; model 3: age, sex, and total energy intake). Our results suggest a strong association between sodium intake and abdominal obesity in pre-diabetes Korean adults.
Yingjuan, Liang;Jinpeng, Wang;Xinyu, Li;Shuang, Wu;Chaoqian, Jiang;Yue, Wang;Xuechun, Li;Zhong-Hua, Liu;Yanshuang, Mu
Journal of Veterinary Science
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v.23
no.6
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pp.90.01-90.13
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2022
Background: Insulin regulates glucose homeostasis and has important effects on metabolism, cell growth, and differentiation. Depending on the cell type and physiological context, insulin signal has specific pathways and biological outcomes in different tissues and cells. For studying the signal pathway of insulin on glycolipid metabolism in porcine embryonic fibroblast (PEF), we used high-throughput sequencing to monitor gene expression patterns regulated by insulin. Objectives: The goal of our research was to see how insulin affected glucose and lipid metabolism in PEFs. Methods: We cultured the PEFs with the addition of insulin and sampled them at 0, 48, and 72 h for RNA-Seq analysis in triplicate for each time point. Results: At 48 and 72 h, 801 and 1,176 genes were differentially expressed, respectively. Of these, 272 up-regulated genes and 264 down-regulated genes were common to both time points. Gene Ontology analysis was used to annotate the functions of the differentially expressed genes (DEGs), the biological processes related to lipid metabolism and cell cycle were dominant. And the DEGs were significantly enriched in interleukin-17 signaling pathway, phosphatidylinositol-3-kinase-protein kinase B signaling pathway, pyruvate metabolism, and others pathways related to lipid metabolism by Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Conclusions: These results elucidate the transcriptomic response to insulin in PEF. The genes and pathways involved in the transcriptome mechanisms provide useful information for further research into the complicated molecular processes of insulin in PEF.
BACKGROUND/OBJECTIVES: Diabetes-specific oral nutritional supplements (ONS) have anti-hyperglycemic effects, while D-allulose exerts anti-diabetic and anti-obesity effects. In this study, we investigated the efficacy and safety of diabetes-specific ONS, including allulose, on glycemic and weight changes in overweight or obese patients with type 2 diabetes mellitus (T2DM). SUBJECTS/METHODS: A single-arm, historical-control pilot clinical trial was conducted on 26 overweight or obese patients with T2DM (age range: 30-70 yrs). The participants were administered 2 packs of diabetes-specific ONS, including allulose (200 kcal/200 mL), every morning for 8 weeks. The glycemic profiles, obesity-related parameters, and lipid profiles were assessed to evaluate the efficacy of ONS. RESULTS: After 8 weeks, fasting blood glucose (FBG) level significantly decreased from 139.00 ± 29.66 mg/dL to 126.08 ± 32.00 mg/dL (P = 0.007) and glycosylated hemoglobin (HbA1c) improved (7.23 ± 0.82% vs. 7.03 ± 0.69%, P = 0.041). Moreover, the fasting insulin (δ: -1.81 ± 3.61 μU/mL, P = 0.017) and homeostasis model assessment for insulin resistance (HOMA-IR) (δ: -0.87 ± 1.57, P = 0.009) levels decreased at 8 weeks, and body weight significantly decreased from 67.20 ± 8.29 kg to 66.43 ± 8.12 kg (P = 0.008). Body mass index (BMI) also decreased in accordance with this (from 25.59 ± 1.82 kg/m2 to 25.30 ± 1.86 kg/m2, P = 0.009), as did waist circumference (δ: -1.31 ± 2.04 cm, P = 0.003). CONCLUSIONS: The consumption of diabetes-specific ONS with allulose in overweight or obese patients with T2DM improved glycemic profiles, such as FBG, HbA1c, and HOMA-IR, and reduced body weight and BMI.
Background: Hepatic lipid disorder impaired mitochondrial homeostasis and intracellular redox balance, triggering development of non-alcohol fatty liver disease (NAFLD), while effective therapeutic approach remains inadequate. Ginsenosides Rc has been reported to maintain glucose balance in adipose tissue, while its role in regulating lipid metabolism remain vacant. Thus, we investigated the function and mechanism of ginsenosides Rc in defending high fat diet (HFD)-induced NAFLD. Methods: Mice primary hepatocytes (MPHs) challenged with oleic acid & palmitic acid were used to test the effects of ginsenosides Rc on intracellular lipid metabolism. RNAseq and molecular docking study were performed to explore potential targets of ginsenosides Rc in defending lipid deposition. Wild type and liver specific sirtuin 6 (SIRT6, 50721) deficient mice on HFD for 12 weeks were subjected to different dose of ginsenosides Rc to determine the function and detailed mechanism in vivo. Results: We identified ginsenosides Rc as a novel SIRT6 activator via increasing its expression and deacetylase activity. Ginsenosides Rc defends OA&PA-induced lipid deposition in MPHs and protects mice against HFD-induced metabolic disorder in dosage dependent manner. Ginsenosides Rc (20mg/kg) injection improved glucose intolerance, insulin resistance, oxidative stress and inflammation response in HFD mice. Ginsenosides Rc treatment accelerates peroxisome proliferator activated receptor alpha (PPAR-α, 19013)-mediated fatty acid oxidation in vivo and in vitro. Hepatic specific SIRT6 deletion abolished ginsenoside Rc-derived protective effects against HFD-induced NAFLD. Conclusion: Ginsenosides Rc protects mice against HFD-induced hepatosteatosis by improving PPAR-α-mediated fatty acid oxidation and antioxidant capacity in a SIRT6 dependent manner, and providing a promising strategy for NAFLD.
Purpose: Obesity is rapidly increasing in Korean children. Obesity is a risk factor for cardiovascular morbidity and is frequently associated with hypertension, diabetes mellitus and coronary artery disease. This study was designed to evaluate risk factors of the metabolic syndrome in obese children. Methods: From February 2000 to June 2004, eighty eight obese (body mass index ${\geq}95th$ percentile) children aged 4 to 15 years were included. We measured serum lipid levels (total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol), fasting sugar levels and insulin levels. Insulin resistance was determined by homeostasis model assessment, fasting insulin/glucose ratio and quantitative insulin sensitivity check index. Results: Clustering of risk factors for the metabolic syndrome in obese children demonstrated that 60.2% had more than one risk factors. Hypertension (14.8%), hypertriglyceridemia (14.8%), HDL-hypocholesterolemia (14.8%), LDL-hypercholesterolemia (12.5%) and hyperinsulinemia (12.5%) were observed. As BMI increased, there was statistically significant increase in systolic blood pressure, insulin and insulin resistance values. Insulin resistance was correlated to systolic blood pressure, serum lipid and insulin levels. The more risk factors for the metabolic syndrome obese children had, the higher was their insulin resistance. Conclusion: The increase in insulin resistance and clustering of risk factors for the metabolic syndrome are already apparent in obese children. Monitoring these risk factors for the metabolic syndrome should become a part of routine medical care for obese children.
Peroxisome proliferator activated receptor (PPAR)-$\alpha$ of three PPAR subtypes ($-\alpha,\;-\beta/-\gamma,\;-\delta$), which are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors, plays a key role in lipoprotein and glucose homeostasis. A variation in the PPAR-a gene expression has been suggested to influence the development of metabolic syndrome through alterations in lipid concentrations. The aim of our study was to investigate the association between the PPAR-a and metabolic syndrome among South Korean. A total of 542 health screen examinees were enrolled in this study who were examined in Kosin University Gospel Hospital from December, 2004 to July, 2005. The height, weight, waist circumference, and systolic and diastolic blood pressure of the subjects were examined and fasting blood glucose, total cholesterol, HDL cholesterol, LDL cholesterol, triglyceride were measured by-sampling in venous blood. The metabolic syndrome was defined as the presence of three or more of the following : waist circumference men ${\geq}90cm$, women ${\geq}80cm$, blood pressure ${\geq}130/85mmHg$, fasting glucose ${\geq}110mg/dL$, HDL cholesterol men <40 mg/dL, women <50 mg/dL, triglyceride ${\geq}150mg/dL$. The blood pressure, fasting glucose, HDL cholesterol, triglyceride were evaluated by using the criteria of NECP ATP III and waist circumference was assessed by using the criteria of WHO Asia-Western Pacific. And the author compared the frequency of the PPAR-$\alpha$ mutation of L162V ($C{\rightarrow}G$ variant in exon 5) in a sample of 542 subjects with and without the metabolic syndrome by polymerase chain reaction allele-specific oligonucleotide (PCR-ASO) method. One (0.2%) hetero-isotype among high risk of metabolic syndrome was identified. The values of waist circumference, body mass index and low density lipoprotein cholesterol of the mutant were 100 cm, 28.6 $kg/m^2$ and 120 mg/dL, respectively. Although the author failed to see significant association between the presence of the PPAR-$\alpha$ L162V polymorphism and metabolic syndrome, one PPAR-$\alpha$ L162V polymorphism in metabolic syndrome patients was found.
Purpose : Adiponectin, adipose tissue-specific protein, has anti-inflammatory and anti-atherogenic properties. It has been found to have a negative correlation with obesity and to play a role in modulating glucose tolerance and insulin sensitivity. Serum adiponectin concentrations are decreased in adults with obesity and type 2 diabetes. We investigated the difference in adiponectin levels between obese and non-obese children, and evaluated the relationship of serum adiponectin with body mass index(BMI), serum fasting insulin, lipid profiles and homeostasis model assessment(HOMA) in children. Methods : We measured serum adiponectin levels by radioimmunoassay in 113 children(82 obese children and 31 non-obese controls) from 8 to 15 years of age, and also checked BMI, fasting serum glucose, insulin and lipid profiles. Fasting and postprandial serum adiponectin concentrations were compared by oral glucose tolerance tests in 27 obese children. The correlations of adiponectin with BMI, insulin, low density lipoprotein(LDL)-cholesterol and HOMA were analyzed by Pearson's correlation. Results : The serum adiponectin levels were significantly lower in the obese group(19.7 mg/mL) than in the non-obese group(27.5 mg/mL)(P<0.01). Serum adiponectin concentrations were negatively correlated with BMI(r=-0.39, P<0.01), serum insulin(r=-0.28, P<0.01), LDL-C(r=-0.20, P<0.01) and HOMA(r=-0.22, P<0.01). At oral glucose tolerance tests in obese children, postprandial 2 hours adiponectin level(19.8 mg/mL) was decreased compared to fasting level(25.8 mg/mL)(P<0.01). Conclusion : Serum adiponectin concentrations were inversely related to adiposity and insulin resistance in children. We suggest the serum adiponectin level could be used as an early marker of insulin resistance in obese children.
Purpose : This study investigated the clinical significance of AN in children and adolescents with obesity induced metabolic complications. Methods : Forty-nine patients who had obesity induced metabolic complications were participated in this cross-sectional study. Obesity induced metabolic complications are as follows: hypertension, dyslipidemia, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), nonalcoholic steatohepatitis (NASH), homeostasis model assessment of insulin resistance (HOMA-IR)>3.16. Clinical characteristics, such as, age, percentage-weight-for-height (PWH), pubertal status, blood pressure (BP), fasting plasma insulin level, fasting and post-oral glucose tolerance test 2-hour glucose levels, liver function test, lipid profile, HOMA-IR were compared according to the presence of AN. Results : Sixty-five percent of patients had AN, 57.1% NASH, 57.1% dyslipidemia, 55.1% hypertension, 46.9% IFG, 24.5% HOMA-IR>3.16 and 16.2% IGT. The patients who were moderately to severely obese with AN had higher incidence of IGT and HOMA-IR>3.16. The patients with AN had significantly higher diastolic BP ($79.4{\pm}6.9$ vs $75.4{\pm}5.6mmHg$), fasting levels of plasma insulin ($10.6{\pm}6.0$ vs $6.2{\pm}5.4{\mu}IU/mL$), HOMA-IR index ($2.6{\pm}1.4$ vs $1.4{\pm}1.3$) and PWH ($42.4{\pm}13.0$ vs $34.3{\pm}1.8%$). The increasing tendency for the presence of AN was significantly related to the cumulative number of obesity induced metabolic complications. Binary logistic regression analysis revealed that the presence of AN was significantly associated with fasting plasma insulin level, PWH and IFG. Conclusion : AN could be useful as a clinical surrogate of obesity induced metabolic complications.
Muscle mass improvement through lifestyle modification has been shown to reduce the risk of metabolic syndrome. This study examined the capacity of ethanol extracts of Scytosiphon lomentaria (SLE) to suppress the bioactivity of myostatin, a potent negative regulator of skeletal muscle mass, as well as the effect of SLE treatment on metabolic homeostasis in obese zebrafish induced by high feeding. A total of 10 ㎍/ml SLE completely blocked myostatin (1 nM/ml) signaling in the pGL3-(CAGA)12 luciferase assay and suppressed myostatin-induced Smad2 phosphorylation in the Western blot analysis. In the zebrafish larvae analysis, the whole body glucose concentration of the high feeding control (HFC) group was significantly higher than that of the normal feeding control (NFC) group. However, the glucose levels of the high feeding group treated with 12.5 ug SLE and of the high feeding group treated with 18.75 ug SLE were similar to those of the NFC group. The mRNA expression level of the GLUT2 gene of the HFC group was significantly lower than that of the NFC group. SLE treatment restored the expression of the GLUT2 gene to a level that was close to that of the NFC group, indicating that SLE is capable of regulating glucose levels in zebrafish larvae. The current results highlight the potential of SLE as a natural MSTN inhibitor and supplement that can be used to facilitate the treatment of metabolic syndrome.
Background: As a process of aging, skeletal muscle mass and function gradually decrease. It is reported that ginsenoside Rb1 and Rb2 play a role as AMP-activated protein kinase activator, resulting in regulating glucose homeostasis, and Rb1 reduces oxidative stress in aged skeletal muscles through activating the phosphatidylinositol 3-kinase/Akt/Nrf2 pathway. We examined the effects of Rb1 and Rb2 on differentiation of the muscle stem cells and myotube formation. Methods: C2C12 myoblasts treated with Rb1 and/or Rb2 were differentiated and induced to myotube formation, followed by immunoblotting for myogenic marker proteins, such as myosin heavy chain, MyoD, and myogenin, or immunostaining for myosin heavy chain or immunoprecipitation analysis for heterodimerization of MyoD/E-proteins. Results: Rb1 and Rb2 enhanced myoblast differentiation through accelerating MyoD/E-protein heterodimerization and increased myotube hypertrophy, accompanied by activation of Akt/mammalian target of rapamycin signaling. In addition, Rb1 and Rb2 induced the MyoD-mediated transdifferentiation of the rhabdomyosarcoma cells into myoblasts. Furthermore, co-treatment with Rb1 and Rb2 had synergistically enhanced myoblast differentiation through Akt activation. Conclusion: Rb1 and Rb2 upregulate myotube growth and myogenic differentiation through activating Akt/mammalian target of rapamycin signaling and inducing myogenic conversion of fibroblasts. Thus, our first finding indicates that Rb1 and Rb2 have strong potential as a helpful remedy to prevent and treat muscle atrophy, such as age-related muscular dystrophy.
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