Obesity increases the risks of diabetes, hypertension, and cardiovascular diseases, ultimately contributing to mortality. Korean Society for the Study of Obesity (KSSO) was established to improve the management of obesity through research and education; to that end, the Committee of Clinical Practice Guidelines of KSSO reviews systemic evidence using expert panels to develop clinical guidelines. The clinical practice guidelines for obesity were revised in 2018 using National Health Insurance Service Health checkup data from 2006 to 2015. Following these guidelines, we added a category, class III obesity, which includes individuals with body mass index (BMI) ≥35 kg/m 2 . Agreeing with the International Federation for the Surgery of Obesity and Metabolic Disorders, Asian Pacific Chapter consensus, we determined that bariatric surgery is indicated for Korean patients with BMI ≥35 kg/m 2 and for Korean patients with BMI ≥30 kg/m 2 who have comorbidities. The new guidelines focus on guiding clinicians and patients to manage obesity more effectively. Our recommendations and treatment algorithms can serve as a guide for the evaluation, prevention, and management of overweight and obesity.

Obesity is a prevalent and complex disease. The prevalence of obesity in Korea increased from 29.7% in 2010 to 35.7% in 2018, with the prevalence of abdominal obesity among Korean adults in 2018 being 23.8%. Obesity contributes to medical costs and socio-economic burden due to associated comorbidities. The treatment and management of obesity is changing and reflects new clinical evidence. The 2020 Korean Society for the Study of Obesity Guideline for the Management of Obesity in Korea summarizes evidence-based recommendations and treatment guidelines.

Background The prevalence of obesity and related comorbidities is increasing worldwide, including in Korea. The Korean Society for the Study of Obesity released the Obesity Fact Sheet 2017 to address this problem in the Korean population. Methods Data from the National Health Insurance Service Health Checkup database from 2006 to 2015 were standardized by age and sex using the 2010 Census. The definition of obesity was a body mass index (BMI) ≥25 kg/m 2 , and that of abdominal obesity was a waist circumference ≥90 cm in men and ≥85 cm in women. Multivariate adjusted Cox regression analysis was conducted, and hazard ratios (HRs) with 95% confidence intervals were calculated for comorbidities. Results From 2009 to 2015, the prevalence of obesity increased from 29.7% to 32.4%, and that of abdominal obesity increased from 18.4% to 20.8%. Obesity with abdominal obesity also increased from 15.1% to 17.7%. Between 2014 and 2015, the prevalence of obesity increased until 30–40 years of age, but decreased from 40–50 years of age in men. In women, it increased until the mid-70s, and decreased thereafter. Abdominal obesity increased from 20–30 years of age to 70–80 years of age, but decreased thereafter. The HRs for type 2 diabetes mellitus, hypertension, dyslipidemia, myocardial infarction, and ischemic stroke were elevated in subjects with abdominal obesity, and their incidence increased as the BMI increased, but slowed down at BMI ≥35 kg/m 2 . Conclusion Based on the Obesity Fact Sheet 2017, strategies for reducing the prevalence of obesity and abdominal obesity are essential.

Background: The prevalence of obesity has rapidly increased in countries across the world in recent decades.

We analyzed the in vivo tumor regression activity of high molecular mass poly-γ-glutamate (γ-PGA) from Bacillus subtilis sups. chungkookjang. C57BL/6 mice were orally administered 10-, 100-, or 2000-kDa γ-PGA or β-glucan (positive control), and antitumor immunity was examined. Our results revealed higher levels of NK cell-mediated cytotoxicity and IFN-γ secretion in mice treated with higher molecular mass γ-PGA (2000 kDa) vs those treated with lower molecular mass γ-PGA (10 or 100 kDa) or β-glucan. We then examined the effect of oral administration of 10- or 2000-kDa γ-PGA on protection against B16 tumor challenge in C57BL/6 mice. Mice receiving high molecular mass γ-PGA (2000 kDa) showed significantly smaller tumor sizes following challenge with the MHC class I-down-regulated tumor cell lines, B16 and TC-1 P3 (A15), but not with TC-1 cells, which have normal MHC class I expression. Lastly, we found that γ-PGA-induced antitumor effect was decreased by in vivo depletion of NK cells using mAb PK136 or anti-asialo GM1 Ab, and that was completely blocked in NK cell-deficient B6 beige mice or IFN-γ knockout mice. Taken together, we demonstrated that oral administration of high molecular mass γ-PGA (2000 kDa) generated significant NK cell-mediated antitumor activity in mice bearing MHC class I-deficient tumors.

Previous studies have suggested that diabetes increases the risk of Parkinson disease (PD); however, this has not been conclusively established. We analyzed the risk of PD based on baseline glucose tolerance status in a large-scale cohort representative of the general Korean population. RESEARCH DESIGN AND METHODS This analysis was performed in a cohort of 15,168,021 adults aged ‡40 years who underwent health checkups under the National Health Insurance Service between January 2009 and December 2010. The clinical course of subjects was monitored until December 2016. Subjects were classified into the following groups: no diabetes, impaired fasting glucose (IFG), diabetes duration <5 years, and diabetes duration ‡5 years. We analyzed the adjusted hazard ratio of PD for each group. RESULTS During the observation period of 49,076,148.74 person-years, PD occurred in 31,577 patients. Compared with the nondiabetes group, the adjusted hazard ratio was 1.038 (95% CI, 1.009-1.067) in the IFG group, 1.185 (95% CI, 1.143-1.229) in the diabetes duration <5 years group, and 1.618 (95% CI, 1.566-1.672) in the diabetes duration ‡5 years group. These results were consistent with those of the subgroup analysis, and the presence of diabetes further increased the risk of PD regardless of comorbidities such as cardiovascular, cerebrovascular, and chronic kidney diseases. CONCLUSIONS This population-based cohort study suggests that diabetes is an independent risk factor for PD. The prevalence of diabetes and related complications is increasing worldwide (1,2). Accordingly, the burden on global health care related to diabetes continues to increase (1,3). Meanwhile, various therapeutic interventions for diabetes have been developed, and the clinical course and quality of life of people with diabetes have improved (4). However, it remains impossible to completely prevent the development of diabetes-related complications. Rather, the clinical significance of previously overlooked atypical complications has paradoxically increased (5). Parkinson disease (PD) is also a major chronic disease, and its clinical significance is increasing worldwide. Damage to the dopaminergic neurons of the substantia nigra is known to be a major cause of PD, which is clinically characterized by a variety of

Previously, we reported that the oral administration of high molecular mass poly-gamma-glutamate (gamma-PGA) induced antitumor immunity but the mechanism underlying this antitumor activity was not understood. In the present study, we found that application of high molecular mass gamma-PGA induced secretion of tumor necrosis factor (TNF)-alpha from the bone-marrow-derived macrophages of wild type (C57BL/6 and C3H/HeN) and Toll-like receptor 2 knockout (TLR2(-/-)) mice, but not those of myeloid differentiation factor 88 knockout (MyD88(-/-)) and TLR4-defective mice (C3H/HeJ). Production of interferon (IFN)-gamma-inducible protein 10 (IP-10) in response to treatment with gamma-PGA was almost abolished in C3H/HeJ mice. In contrast to LPS, gamma-PGA induced productions of TNF-alpha and IP-10 could not be blocked by polymyxin B. Furthermore, gamma-PGA-induced interleukin-12 production was also impaired in immature dendritic cells (iDCs) from MyD88(-/-) and C3H/HeJ mice. Downregulation of MyD88 and TLR4 expression using small interfering RNA (siRNA) significantly inhibited gamma-PGA-induced TNF-alpha secretion from the RAW264.7 cells. Gamma-PGA-mediated intracellular signaling was markedly inhibited in C3H/HeJ cells. The antitumor effect of gamma-PGA was completely abrogated in C3H/HeJ mice compared with control mice (C3H/HeN) but significant antitumor effect was generated by the intratumoral administration of C3H/HeN mice-derived iDCs followed by 2,000 kDa gamma-PGA in C3H/HeJ. These findings strongly suggest that the antitumor activity of gamma-PGA is mediated by TLR4.

Lee 4,* , on behalf of the Taskforce Team of the Obesity Fact Sheet of the Korean Society for the Study of Obesity