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Background: There is an international consensus among experts advocating for the classification of fatty liver disease as a metabolic condition. However, some authors have raised concerns that this metabolic-centric framing may result in the underdiagnosis of metabolicdysfunctionassociated steatotic liver disease (MASLD) in lean individuals. The present study was carried out with the objective of describing metabolic characteristics in MASLD and the prevalence of lean MASLD in the general population. Methods: We carried out a hospital-based cross-sectional study. A pre-tested proforma was used to collect data on socio-demographic factors, lifestyle factors, and medical history. Transient elastography and blood investigations were carried out in all patients. The identification of independent predictors for MASLD and liver fibrosis was carried out using multivariable logistic regression. A test of interaction was conducted for studying effect modification in the association of diabetes and MASLD by subgroups of body mass index (BMI). Results: A total of 1,243 participants were interviewed and screened for MASLD. The overall prevalence of MASLD was 43.7% (n = 543), with the prevalence of lean MASLD being 4.3% (n = 53). The prevalence of MASLD in lean vs non-lean subjects differed (21.3 vs 66.7%, p < 0.001). Of the total MASLD cases, lean MASLD constituted 9.7% of cases. The association of diabetes and MASLD did not differ in subgroups by BMI. The test for interaction to detect effect modification was not statistically significant (p = 0.673). Conclusion: The results support laying emphasis on metabolic dysfunction as a key criterion when defining fatty liver disease. The findings emphasize the shared metabolic underpinnings between lean and non-lean MASLD and advocate for inclusive approaches in diagnosis, management, and public health initiatives. [ABSTRACT FROM AUTHOR]

Background and Aims: Schizophrenia spectrum and other psychotic disorders are common disorders often requiring long-term treatment with atypical antipsychotics, which might cause metabolic dysfunctions. We aimed to study the metabolic dysfunctions with olanzapine and risperidone in patients with schizophrenia spectrum and other psychotic disorders. We also explored the incidence of new-onset metabolic syndrome and its predictors. Methods: This was a 24-week prospective observational study conducted at a teaching hospital in North India. The patients were prescribed olanzapine or risperidone. Anthropometric measurements (waist circumference, weight, body mass index, blood pressure) and biochemical investigations (triglycerides, high-density lipoproteins, fasting plasma glucose) were recorded at baseline and after 24 weeks. Metabolic syndrome was defined using the International Diabetes Federation definition. Statistical tests used were Fisher's exact test, paired t-test, unpaired t-test, and logistic regression. Results: A total of 45 patients, 30 on olanzapine and 15 on risperidone completed the study. Statistically significant changes occurred in all variables with olanzapine while with risperidone statistically significant changes occurred in all variables except waist circumference and fasting plasma glucose. Statistically greater changes in mean values between the two were noted only for high-density lipoprotein with olanzapine. 20% of patients developed metabolic syndrome with non-significant between drug differences. Baseline triglyceride predicted the development of the metabolic syndrome. Conclusions: Olanzapine and risperidone cause metabolic derangements and statistically significant differences may not exist between them. Baseline triglyceride levels might predict subsequent metabolic syndrome. [ABSTRACT FROM AUTHOR]