The aim of this study was to develop consensus definitions and diagnostic criteria for sarcopenic obesity tailored to Asia-Oceania populations, a condition characterized by reduced skeletal muscle mass and function with excess adipose tissue. Experts from various fields formed a working group under the Asia-Oceania Association for the Study of Obesity (AOASO) and the International Association of Gerontology and Geriatrics Asia/Oceania Region (IAGG-AOR). The group convened four meetings, employing the Delphi technique to achieve consensus on diagnostic criteria and management strategies for sarcopenic obesity. The consensus defines sarcopenic obesity with a 3-step algorithm, including screening, diagnosis, and intervention. The screening criteria included BMI and waist circumference for obesity and calf circumference, the SARC-F, and the Finger Ring test for sarcopenia. The diagnostic criteria for sarcopenia include assessments of muscle mass (using dual-energy X-ray absorptiometry or bioelectrical impedance analysis), muscle strength (handgrip strength), and physical performance (gait speed, Short Physical Performance Battery, or the 5-Times Sit-to-Stand Test). Central obesity is the main concern for the diagnosis of obesity. The working group recommends a combination of dietary consultations, increased physical activity, resistance training, and the potential use of oral nutritional supplements and medications for managing sarcopenic obesity. The primary objective is to increase skeletal muscle mass and reduce adipose tissue mass. The established criteria facilitate early recognition and management of sarcopenic obesity, highlighting the need for tailored interventions. Future research should focus on the long-term outcomes of these interventions and the development of pharmacological treatments.

Periodontitis and nonalcoholic fatty liver disease (NAFLD) are two prevalent non-communicable diseases affecting people worldwide. The delicate interplay between oral microbiome, intestinal barrier, immune system, and liver is susceptible to disruption by environmental and genetic factors which could result in the onset of systemic diseases. The oral-liver and liver-gut axes have been proposed as the possible mechanisms to explain the links among these factors. Many evidences are mounting to support the role of imbalanced interactions between microbiota and immune system in the development of immune-mediated diseases. The emerging concept of the oral-gut-liver axis is gaining recognition as a means to explore the interconnections among NAFLD, periodontitis, and gut dysbiosis. There is substantial evidence indicating that oral and gut dysbiosis are the significant risk factors for liver disease. Therefore, the role of inflammatory mediators in linking these organs cannot be overlooked. Understanding these complex relationships is crucial in the development of effective strategies for the prevention and management of liver diseases.

Previous studies have suggested that peptic ulcer disease (PUD) including stomach and duodenal ulcers might be associated with periodontitis (PD); however, no clear conclusions have been reached thus far. In this retrospective case-control study, we aimed to investigate the association between PUD and PD by using a large population-based dataset in Taiwan. A population-based retrospective case control study was conducted using the Longitudinal Health Insurance Database 2010 (LHID2010) derived from the National Health Insurance Research database (NHIRD) in Taiwan from 2000 to 2013. The case and control group were matched with gender, age, urbanization level, socioeconomic status, and Charlson comorbidity index (CCI) by using the propensity score method at a 1:1 ratio. A total of 177,240 cases and 177,240 control patients were included in this study, with an average age of 46.96 $\pm$ 11.76 years. The risk of PUD for patients diagnosed with PD was 1.15-fold when compared with those without PD (OR, 1.15; 95% CI, 1.12–1.18). This population-based case control study demonstrated a significantly positive association between PUD and PD in Taiwan.

Obesity and chronic periodontitis are the prevalent chronic conditions significantly linked through shared common inflammatory and immune mechanisms. This review aimed to synthesize current knowledge on the association between obesity and chronic periodontitis, exploring biological mechanisms, epidemiological evidence, and clinical relevance. Obesity induces systemic low-grade inflammation marked by elevated pro-inflammatory cytokines, altered immune responses, and disrupted adipokine profiles that may influence periodontal inflammation. Conversely, chronic periodontitis, characterized by oral microbial dysbiosis and local inflammation, contributes to systemic inflammatory burden and potentially exacerbates obesity-related complications. Obesity-associated dietary habits further promote pathogenic oral microbiome shifts as well as aggravate periodontal inflammation. Clinically, obese patients frequently exhibit more severe chronic periodontitis and diminished responsiveness to conventional periodontal therapies, highlighting the need for tailored clinical interventions and integrated healthcare approaches. Public health efforts should make dental care easier to access, support teamwork between health professionals, and offer clear education to help manage both obesity and chronic periodontitis. Although researches have advanced significantly, the exact causal mechanisms still remain unclear. Further studies are needed to improve prevention as well as treatment strategies, ultimately reducing the global burden of obesity and chronic periodontitis.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent, especially among individuals with type 2 diabetes mellitus. Insulin resistance (IR) is a key shared mechanism. This study aimed to investigate the association between MASLD and IR in individuals with normal glucose levels. We recruited participants from communities and outpatient clinics in central and northern Taiwan, excluding those with impaired fasting glucose or type 2 diabetes mellitus. Data collected included body mass index, blood pressure, body fat percentage, and lifestyle factors. After overnight fasting, blood samples were taken. MASLD was diagnosed via abdominal ultrasonography. IR was calculated using the homeostasis model assessment of insulin resistance formula and categorized into tertiles (T1–T3). Statistical analyses included analysis of variance and multivariate logistic regression. Among 485 participants (mean age 42.0 ± 11.4 years), MASLD prevalence increased with IR levels (T1: 34.1%, T2: 40.1%, T3: 47.8%; P < .001). Fasting glucose remained within normal limits but rose with IR (T1: 81.9 ± 7.4, T2: 85.1 ± 7.6, T3: 87.3 ± 6.5 mg/dL; P < .0001). After adjusting for age, sex, body mass index, exercise, alcohol use, and smoking, MASLD risk was significantly higher in T3 (odds ratio: 3.87, 95% confidence interval: 2.08–7.21) and T2 (odds ratio: 1.83, 95% confidence interval: 1.11–3.00) compared to T1. Even among individuals with normal glucose levels, elevated IR is significantly associated with higher MASLD risk. Early identification and intervention for IR may help prevent MASLD progression.