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Understanding Adipose Tissue Dysfunction.
J Obes Metab Syndr
December 2024
Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany.
Diseases affecting adipose tissue (AT) function include obesity, lipodystrophy, and lipedema, among others. Both a lack of and excess AT are associated with increased risk for developing diseases including type 2 diabetes mellitus, hypertension, obstructive sleep apnea, and some types of cancer. However, individual risk of developing cardiometabolic and other 'obesity-related' diseases is not entirely determined by fat mass.
View Article and Find Full Text PDFGenetic Risk Phenotypes for Type 2 Diabetes Differ with Ancestry in US Adults with Diabetes and Overweight/Obesity.
Arch Med Res
November 2024
Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, USA.
Article Synopsis
- Type 2 diabetes (T2D) risk is notably higher among non-Hispanic black (NHB) and Hispanic individuals, and this study investigates whether genetic factors contribute to these racial disparities.
- The research involved analyzing genetic risk scores associated with T2D pathways in a sample of 361 US adults, revealing that NHB participants exhibited higher scores for β-cell and proinsulin function, suggesting significant differences in T2D etiology among racial groups.
- The findings indicate that impaired β-cell function is a key factor for NHB individuals, while issues such as liver dysfunction and insulin resistance are more prevalent in both NHB and Hispanic populations, potentially guiding future personalized treatment strategies for T2D.
Hepatic SerpinA1 improves energy and glucose metabolism through regulation of preadipocyte proliferation and UCP1 expression.
Nat Commun
November 2024
Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuoku, Kumamoto, Japan.
Lipodystrophy and obesity are associated with insulin resistance and metabolic syndrome accompanied by fat tissue dysregulation. Here, we show that serine protease inhibitor A1 (SerpinA1) expression in the liver is increased during recovery from lipodystrophy caused by the adipocyte-specific loss of insulin signaling in mice. SerpinA1 induces the proliferation of white and brown preadipocytes and increases the expression of uncoupling protein 1 (UCP1) to promote mitochondrial activation in mature white and brown adipocytes.
View Article and Find Full Text PDFThe evolving landscape of ER-LD contact sites.
Front Cell Dev Biol
October 2024
Department of Biotechnology, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Lipid droplets (LDs) are evolutionarily conserved dynamic organelles that play an important role in cellular physiology. Growing evidence suggests that LD biogenesis occurs at discrete endoplasmic reticulum (ER) subdomains demarcated by the lipodystrophy protein, Seipin, lack of which impairs adipogenesis. However, the mechanisms of how these domains are selected is not completely known.
View Article and Find Full Text PDFPhenotypic and molecular reanalysis of a cohort of patients with monogenic diabetes reveals a case of partial lipodystrophy due to the A8344G mutation in the mitochondrial DNA.
Arch Endocrinol Metab
October 2024
Hospital das Clínicas Faculdade de Medicina Universidade de São Paulo São PauloSP Brasil Grupo de Diabetes Monogênico, Unidade de Endocrinologia Genética (LIM25), Unidade de Diabetes, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
Familial partial lipodystrophy (FPLD) is a very rare genetic disease characterized by insulin resistance due to a loss of subcutaneous fat from the extremities together with a progressive storage of fat around the face and neck and inside the abdomen. In over 50% of cases, molecular genetic testing reveals pathogenic variants in two nuclear genes, LMNA and PPARG. The case reported here refers to a woman phenotypically diagnosed with FPLD, who presented with diabetes and multiple cervical lipomatosis and in whom no variant had been found in the nuclear genes classically associated with this syndrome that could explain her phenotype.
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