Adipose Morphology: a Critical Factor in Regulation of Human Metabolic Diseases and Adipose Tissue Dysfunction
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REVIEW
Adipose Morphology: a Critical Factor in Regulation of Human Metabolic Diseases and Adipose Tissue Dysfunction Fangcen Liu 1 & Jielei He 2 & Hongdong Wang 2 & Dalong Zhu 1,2 & Yan Bi 2 Received: 4 May 2020 / Revised: 12 September 2020 / Accepted: 15 September 2020 # The Author(s) 2020
Abstract Emerging evidence highlights that dysfunction of adipose tissue contributes to impaired insulin sensitivity and systemic metabolic deterioration in obese state. Of note, adipocyte hypertrophy serves as a critical event which associates closely with adipose dysfunction. An increase in cell size exacerbates hypoxia and inflammation as well as excessive collagen deposition, finally leading to metabolic dysregulation. Specific mechanisms of adipocyte hypertrophy include dysregulated differentiation and maturation of preadipocytes, enlargement of lipid droplets, and abnormal adipocyte osmolarity sensors. Also, weight loss therapies exert profound influence on adipocyte size. Here, we summarize the critical role of adipocyte hypertrophy in the development of metabolic disturbances. Future studies are required to establish a standard criterion of size measurement to better clarify the impact of adipocyte hypertrophy on changes in metabolic homeostasis. Keywords Adipocyte hypertrophy . Obesity . Insulin resistance . Adipose dysfunction
Abbreviations T2D Type 2 diabetes WAT White adipose tissue AT Adipose tissue NAFLD Non-alcoholic fatty liver disease VAT Visceral AT SAT Subcutaneous AT VAS Visceral adipocyte size SAS Subcutaneous adipocyte size APC Adipocyte precursor cells GWAT Gonadal white adipose tissue IWAT Inguinal white adipose tissue ERα Estrogen receptor alpha ERβ Estrogen receptor beta HOMA-IR Homeostasis model assessment of insulin resistance Fangcen Liu is the first author of this review. * Yan Bi [email protected] 1
Department of Endocrinology, Nanjing Drum Tower Hospital Clinical College, Nanjing Medical University, Nanjing, China
2
Department of Endocrinology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China
IS IR IGT NGT IFG AAS FAS MS ALT AST PCOS TNF-α IL-6 IL-1b CCR MCP-1 iNKT CRP MSCs EBF1 HIF-1α PPARγ IGF-1 CEBPα SAA TM4SF1
Insulin-sensitive Insulin resistance Impaired glucose tolerance Normal glucose tolerance Impaired fasting glucose Abdominal adipocyte size Femoral adipocyte size Metabolic syndrome Alanine aminotransferase Aspartate aminotransferase Polycystic ovary syndrome Tumor necrosis factor α Interleukin-6 Interleukin-1b Chemokine CC receptor Monocyte chemoattractant protein 1 Induced natural killer T C-reactive protein Mesenchymal stem cells EBF transcription factor 1 Hypoxia-inducible factor-1α Peroxisome proliferator-activated receptor γ Insulin-like growth factor 1 CCAAT-enhancer-binding proteins α Serum amyloid A Transmembrane 4 L six family member 1
OBES SURG
PI3K PDK1 PKB GLUT4 GSV WNT WISP2 ZFP423 Tcf/Lef BMP4 TGF-β SMAD RXRα PPREs aP2 FATP FAT/CD36 PEPCK LDs GPAT PC PA Fsp27 Cidea IRS IQGAP-1 MAPKK IKK TRPV4 RVD VRAC SWELL
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