This cross-sectional investigation of 6,931 U.S. adults examined the relationship between sitting time and insulin resistance. A primary objective was to evaluate how this relationship was mediated by the following variables: age, sex, race, year of assessment, cigarette smoking, physical activity, body mass index (BMI), and waist circumference. Self-reported sitting time, measured in minutes per day, was the exposure variable. Insulin resistance, indexed by the homeostatic model assessment of insulin resistance (HOMA-IR), was the outcome variable. Data were used from the 2011-2018 National Health and Nutrition Examination Survey (NHANES). Results showed a strong, positive association between sitting time and insulin resistance after adjusting for age, sex, race, and year of assessment (F = 13.3, p < 0.0001). Further controlling for cigarette smoking and physical activity did not alter the significance of the relationship. Adding BMI to the demographic covariates weakened the relationship but did not nullify it; however, the association was no longer significant after adjusting for differences in waist circumference (F = 1.39, p = 0.2563). Overall, waist circumference was a powerful mediating variable between sitting time and insulin resistance.

京都大学 / 新制・課程博士 / 博士(医学) / 甲第24880号 / 医博第5014号 / 新制||医||1068(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 長船 健二, 教授 江木 盛時, 教授 妹尾 浩 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

Polycystic ovary syndrome (PCOS) affects a substantial percentage of reproductive-aged females. Diagnosis criteria include irregular ovulation, elevated androgens, and polycystic ovaries. PCOS often presents with metabolic and reproductive symptoms, with insulin resistance being a symptom that exacerbates metabolic issues. Exercise as a non-pharmacological intervention is featured in the literature on management of PCOS. The objective of this thesis is to explore the role of exercising in mitigating insulin resistance in women with PCOS. A search for relevant articles that included different exercise methods such as high intensity training was completed using CINAHL and Medline. High intensity training appears to have a more comprehensive effect on metabolic levels, though other exercises offer benefits. Further research should include large and diverse sample sizes, longer research duration, and focus on defining an optimal exercise guideline for women with PCOS.

Objective. Similar to obesity, lipodystrophy (LD) causes adipose tissue dysfunction and severe metabolic complications. Growth differentiation factor 15 (GDF15) belongs to the transforming growth factor β superfamily and is dysregulated in metabolic disease including obesity and diabetes mellitus. Circulating levels in LD and the impact of leptin treatment have not been investigated so far. Material and Methods. GDF15 serum levels were quantified in 60 LD patients without human immunodeficiency virus infection and 60 controls matched for age, gender, and body mass index. The impact of metreleptin treatment on circulating GDF15 was assessed in a subgroup of patients. GDF15 mRNA expression was determined in metabolic tissues of leptin-deficient lipodystrophic aP2-nSREBP1c-Tg mice, obese ob/ob mice, and control C57Bl6 mice. Results. Median GDF15 serum concentrations were significantly higher in LD patients (819 ng/L) as compared to the control group (415 ng/L) (p < 0.001). In multiple linear regression analysis, an independent and positive association remained between GDF15 on one hand and age, patient group, hemoglobin A1c, triglycerides, and C-reactive protein on the other hand. Moreover, there was an independent negative association between GFD15 and estimated glomerular filtration rate. Circulating GDF15 was not significantly affected by metreleptin treatment in LD patients. Gdf15 was upregulated in leptin-deficient lipodystrophic mice as compared to controls. Moreover, Gdf15 mRNA expression was downregulated by leptin treatment in lipodystrophic and obese animals. Conclusions. Serum concentrations of GDF15 are elevated in LD patients and independently associated with markers of metabolic dysfunction. Gdf15 expression is higher in lipodystrophic mice and downregulated by leptin treatment.

Objective. Similar to obesity, lipodystrophy (LD) causes adipose tissue dysfunction and severe metabolic complications. Growth differentiation factor 15 (GDF15) belongs to the transforming growth factor superfamily and is dysregulated in metabolic disease including obesity and diabetes mellitus. Circulating levels in LDand the impact of leptin treatment have not been investigated so far.Material and Methods. GDF15 serum levels were quantified in 60 LD patients without human immunodeficiency virus infection and 60 controlsmatched for age, gender, and bodymass index. The impact ofmetreleptin treatment on circulating GDF15 was assessed in a subgroup of patients. GDF15 mRNA expression was determined in metabolic tissues of leptin-deficient lipodystrophic aP2-nSREBP1c-Tg mice, obese ob/ob mice, and control C57Bl6 mice. Results. Median GDF15 serum concentrations were significantly higher in LD patients (819 ng/L) as compared to the control group (415 ng/L) (p < 0.001). In multiple linear regression analysis, an independent and positive association remained between GDF15 on one hand and age, patient group, hemoglobin A1c, triglycerides, and C-reactive protein on the other hand. Moreover, there was an independent negative association between GFD15 and estimated glomerular filtration rate. Circulating GDF15 was not significantly affected by metreleptin treatment in LD patients. Gdf15 was upregulated in leptin-deficient lipodystrophic mice as compared to controls. Moreover, Gdf15 mRNA expression was downregulated by leptin treatment in lipodystrophic and obese animals. Conclusions. Serum concentrations of GDF15 are elevated in LD patients and independently associated withmarkers of metabolic dysfunction. Gdf15 expression is higher in lipodystrophic mice and downregulated by leptin treatment.

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