• The Journal of Internal Korean Medicine
• /
• v.35 no.4
• /
• pp.428-438
• /
• 2014

Objectives: Obesity is an important cause of insulin resistance that leads to obese type 2 diabetes. Recently it has been found that obesity is associated with adipose tissue accumulation which causes systemic inflammation. In this study, we investigated effects of Inula helenium on the inflammation in high fat diet-induced insulin resistance mouse. Methods: Insulin resistance was induced in C57BL/6 male mice (19~21 g) on a 60% fat diet. Mice were divided into 3 groups (n=6) of normal, control and Inula helenium. After 12 weeks, body weight, FBS, oral glucose tolerance test (OGTT), serum level of insulin, epididymal fat pad, liver weight and the gene expression of tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-6, interleukin (IL)-10 and cluster of differentiation (CD) 68 were measured. Also, adipose tissue macrophage was analyzed by fluorescence activated cell sorting. Results: Inula helenium significantly reduces oral glucose tolerance levels, insulin serum level and adipose tissue macrophage. Also Inula helenium increased IL-10 gene expression and decreased CD68 gene expression. Conclusions: These results show that Inula helenium has anti-insulin resistance and anti-inflammatory effects on a high fat diet-induced insulin resistance mouse model.

• Nutrition Research and Practice
• /
• v.8 no.5
• /
• pp.544-549
• /
• 2014

BACKGROUND/OBJECTIVES: Obesity-associated insulin resistance is a strong risk factor for type 2 diabetes mellitus. The aim of this study was to investigate the effect of myricetin on adiposity, insulin resistance, and inflammatory markers in mice with diet-induced insulin resistance. MATERIALS/METHODS: Five-week-old male C57BL/6J mice were fed a basal diet, a high-fat, high-sucrose (HFHS) diet, or the HFHS diet containing 0.06% myricetin or 0.12% myricetin for 12 weeks after a 1-week adaptation, and body weight and food intake were monitored. After sacrifice, serum lipid profiles, glucose, insulin, adipocyte-derived hormones, and proinflammatory cytokines were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was determined. RESULTS: Myricetin given at 0.12% of the total diet significantly reduced body weight, weight gain, and epidydimal white adipose tissue weight, and improved hypertriglyceridemia and hypercholesterolemia without a significant influence on food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, decreased significantly by 0.12% myricetin supplementation in mice fed the HFHS diet. Myricetin given at 0.12% of the total diet significantly reduced serum levels of leptin, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) in mice fed the HFHS diet. CONCLUSIONS: These findings suggest that myricetin may have a protective effect against diet-induced obesity and insulin resistance in mice fed HFHS diet, and that alleviation of insulin resistance could partly occur by improving obesity and reducing serum proinflammatory cytokine levels.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.11 no.sup1
• /
• pp.149-152
• /
• 2008

Obesity tracks from childhood into adulthood, and the persistence of obesity rises with age among obese children. Obesity are independent risk factors for increased morbidity and mortality throughout the lifecycle. Obese individuals develop resistance to the cellular actions of insulin, characterized by an impaired ability of insulin to inhibit glucose output from the liver and to promote glucose uptake in fat and muscle. Insulin resistance is a key etiological factor for type 2 diabetes mellitus, dyslipidemia, hypertension, nonalcoholic steatohepatitis, polycystic ovarian syndrome.

• Journal of the Korea Convergence Society
• /
• v.11 no.10
• /
• pp.155-162
• /
• 2020

This study wanted to confirm the relevance between body mass index(BMI) and insulin resistance and beta-cell function based on abdominal obesity in obese middle-aged men. This study targeted 797 obese middle-aged men who had undergone health checkups at general hospitals in Gyeonggi-do from January 2018 to June 2020. There were 327 in the group with abdominal obesity and 470 in the group without abdominal obesity. Glucose(p<0.001), HbA1c(p=0.003), insulin(p<0.001), HOMA-IR(p<0.001) was different between groups. BMI was a factor affecting insulin resistance and beta cell function regardless of the with or without of abdominal obesity. BMI was associated with the onset of disease of insulin resistance and beta cell functional degradation regardless of the with or without of abdominal obesity. Therefore, it is considered necessary to manage the indicators of the BMI through exercise programs and regular checkups for health management of middle-aged obese men.

• Korean Journal of Community Nutrition
• /
• v.6 no.1
• /
• pp.97-107
• /
• 2001

The clustering of insulin resistance with hypertension, glucose intolerance, hyperinsulinemia, increased triglyceride and decreased HDL cholesterol levels, and central and overall obesity has been called syndrome X, or the insulin resistance syndrome(IRS). To develop a nutrition service for IRS, this study was performed to evaluate the prevalence of each component of the metabolic abnormalities of IRS and analyze the clustering pattern of IRS among subjects living in the Taegu community. Participants in this study were 9234(mean age ; M/F 48/40yrs);63.5% were men, 24.4% were obese, 13.3% had hypertension. 3.7% had hyperglycemia, and 32.4% had hyperlipidemia. The IRS was defined as the coexistence of two or more components among metabolic abnormalities; obesity, hypertension. hyperglucemia and hyperlipidemia. The prevalence of IRS in Taegu was 19.2%(M/F:20.8%/16.4%), the clustering of these fisk variables was higher in advanced age group. Among the subjects of IRS having two of more diseases, 75.6% were obese, the pattern were similar in men and women. The younger, the higher the prevalence of obesity associated clustering patterns. The prevalence of obesity associated patterns among the hyperglycemia associated clustering patterns was 44.5%. The samples of the representative clustering patterns were obesity and hyperlipidemia (8.0%), hypertension and hyperlipidemia(3.2%), hypertension, obesity and hyperlipiemia(3.1%), hypertension and obesity(2.3%), and hyperglycemia and hyperlipidemia(0.8%). The clustering of obesity and hyperlipidemia until 50 year old groups, and the clustering of hypertension and hyperlipidemia in the 60 and 70 age groups were the most prevalent. We concluded that insulin resistance syndrome was a relatively common disorder in the Taegu community, and prevalence and the characteristics of the intervention strategies for IRS are desired, an effective improvement will be achieved.

• IMMUNE NETWORK
• /
• v.22 no.1
• /
• pp.13.1-13.14
• /
• 2022

Chronic inflammation plays a critical role in the development of obesity-associated metabolic disorders such as insulin resistance. Obesity alters the microenvironment of adipose tissue and the intestines from anti-inflammatory to pro-inflammatory, which promotes low grade systemic inflammation and insulin resistance in obese mice. Various T cell subsets either help maintain metabolic homeostasis in healthy states or contribute to obesity-associated metabolic syndromes. In this review, we will discuss the T cell subsets that reside in adipose tissue and intestines and their role in the development of obesity-induced systemic inflammation.

• Journal of Yeungnam Medical Science
• /
• v.38 no.2
• /
• pp.83-94
• /
• 2021

The global obesity epidemic and the growing elderly population largely contribute to the increasing incidence of type 2 diabetes. Insulin resistance acts as a critical link between the present obesity pandemic and type 2 diabetes. Naturally occurring reactive oxygen species (ROS) regulate intracellular signaling and are kept in balance by the antioxidant system. However, the imbalance between ROS production and antioxidant capacity causes ROS accumulation and induces oxidative stress. Oxidative stress interrupts insulin-mediated intracellular signaling pathways, as supported by studies involving genetic modification of antioxidant enzymes in experimental rodents. In addition, a close association between oxidative stress and insulin resistance has been reported in numerous human studies. However, the controversial results with the use of antioxidants in type 2 diabetes raise the question of whether oxidative stress plays a critical role in insulin resistance. In this review article, we discuss the relevance of oxidative stress to insulin resistance based on genetically modified animal models and human trials.

• Journal of Nutrition and Health
• /
• v.35 no.7
• /
• pp.737-742
• /
• 2002

To evaluate the effect of obesity on serum leptin and insulin levels in 80 elementary school children (aged 10.8 yr, 47 boys, 33 girls), we collected the anthropometric data and measured serum leptin and insulin levels. Serum leptin level and insulin resistance are known as factors which are associated with obesity and obesity related diseases such as diabetes, cardiovascular disease, hypertension. The results were as follows. The serum levels of insulin (p＜0.001), leptin (p＜0.001) and HOM $A_{IR}$ (p＜0.001) in obese group were significantly higher than those of other groups. The obesity indices correlated significantly to serum levels of insulin and leptin, but not to fasting glucose level. These results suggested that circulating leptin and insulin concentrations may act as a humoral signal indicator to adiposity-associated metabolic disorder in elementary school children.

• Clinical and Experimental Pediatrics
• /
• v.59 no.5
• /
• pp.231-238
• /
• 2016

Purpose: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute phase protein, derived from the liver, which is present in high concentrations in plasma. Data regarding the association between circulating plasma LBP levels and obesity-related biomarkers in the pediatric population are scarce. We aimed to determine whether there was a difference in plasma LBP levels between overweight/obese and normal-weight adolescents and to assess the correlation of circulating LBP levels with anthropometric measures and obesity-related biomarkers, including insulin resistance, liver enzyme levels, and lipid profiles. Methods: The study included 87 adolescents aged 12-13 years; 44 were overweight/obese and 43 were of normal-weight. We assessed anthropometric and laboratory measures, including body mass index (BMI), blood pressure, insulin resistance, liver enzyme levels, and lipid profiles. Plasma LBP levels were measured using an enzyme-linked immunosorbent assay. Results: The mean age of the participants was $12.9{\pm}0.3$ years. Circulating plasma LBP levels were significantly increased in overweight/obese participants compared with those in normal-weight participants ($7.8{\pm}1.9{\mu}g/mL$ vs. $6.0{\pm}1.6{\mu}g/mL$, P<0.001). LBP levels were significantly and positively associated with BMI, systolic blood pressure, aspartate aminotransferase, alanine aminotransferase, total cholesterol, low density lipoprotein-cholesterol, fasting glucose and insulin, and insulin resistance as indicated by the homeostatic model assessment of insulin resistance (HOMA-IR) (all P<0.05). In multivariate linear regression analysis, BMI and HOMA-IR were independently and positively associated with plasma LBP levels. Conclusion: LBP is an inflammatory biomarker associated with BMI and obesity-related insulin resistance in adolescents. The positive correlation between these parameters suggests a potentially relevant pathophysiological mechanism linking LBP to obesity-related insulin resistance in adolescents.

• IMMUNE NETWORK
• /
• v.11 no.1
• /
• pp.59-67
• /
• 2011

Background: Insulin resistance is an integral feature of metabolic syndromes, including obesity, hyperglycemia, and hyperlipidemia. In this study, we evaluated whether the aloe component could reduce obesity-induced inflammation and the occurrence of metabolic disorders such as blood glucose and insulin resistance. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM lowered fasting blood glucose and plasma insulin compared with HFD. Obesity-induced inflammatory cytokine (IL-$1{\beta}$, -6, -12, TNF-${\alpha}$) and chemokine (CX3CL1, CCL5) mRNA and protein were decreased markedly, as was macrophage infiltration and hepatic triglycerides by Aloe QDM. At the same time, Aloe QDM decreased the mRNA and protein of $PPAR{\gamma}/LXR{\alpha}$ and $11{\beta}$-HSD1 both in the liver and WAT. Conclusion: Dietary aloe formula reduces obesity-induced glucose tolerance not only by suppressing inflammatory responses but also by inducing anti-inflammatory cytokines in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The effect of Aloe QDM complex in the WAT and liver are related to its dual action on $PPAR{\gamma}$ and $11{\beta}$-HSD1 ression and its use as a nutritional intervention against T2D and obesity-related inflammation is suggested.