Familial partial lipodystrophy type 2 and obesity, two adipose tissue pathologies with different inflammatory profiles

[1]  P. Meikle,et al.  Lipoatrophic diabetes in Familial Partial Lipodystrophy type 2: from insulin resistance to diabetes. , 2022, Diabetes & metabolism.

[2]  S. Chon,et al.  Assessment of Insulin Secretion and Insulin Resistance in Human , 2021, Diabetes & metabolism journal.

[3]  C. Vigouroux,et al.  A recurrent familial partial lipodystrophy due to a monoallelic or biallelic LMNA founder variant highlights the multifaceted cardiac manifestations of metabolic laminopathies. , 2021, European Journal of Endocrinology.

[4]  S. Kihara,et al.  Atheroprotective Roles of Adiponectin via CCL2 Inhibition , 2020, Journal of atherosclerosis and thrombosis.

[5]  E. Helfer,et al.  Molecular and Mechanobiological Pathways Related to the Physiopathology of FPLD2 , 2020, Cells.

[6]  N. Lamblin,et al.  Cardiometabolic assessment of lamin A/C gene mutation carriers: A phenotype-genotype correlation. , 2019, Diabetes & metabolism.

[7]  M. Foss,et al.  Endoplasmic reticulum stress activation in adipose tissue induces metabolic syndrome in individuals with familial partial lipodystrophy of the Dunnigan type , 2018, Diabetology & Metabolic Syndrome.

[8]  F. Santini,et al.  Lipodystrophy and obesity are associated with decreased number of T cells with regulatory function and pro-inflammatory macrophage phenotype , 2017, International Journal of Obesity.

[9]  Y. Abed,et al.  Obesity and inflammation: the linking mechanism and the complications , 2016, Archives of medical science : AMS.

[10]  W. D. De Vos,et al.  Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates , 2015, Nucleus.

[11]  Qinghua Sun,et al.  Macrophage recruitment in obese adipose tissue , 2015, Obesity reviews : an official journal of the International Association for the Study of Obesity.

[12]  C. Vigouroux,et al.  Lipodystrophy-Linked LMNA p.R482W Mutation Induces Clinical Early Atherosclerosis and In Vitro Endothelial Dysfunction , 2013, Arteriosclerosis, thrombosis, and vascular biology.

[13]  J. Tanti,et al.  Implication of inflammatory signaling pathways in obesity-induced insulin resistance , 2013, Front. Endocrin..

[14]  B. Venkatesh,et al.  Clinical review: Adiponectin biology and its role in inflammation and critical illness , 2011, Critical care.

[15]  C. Vigouroux,et al.  A homozygous mutation of prelamin-A preventing its farnesylation and maturation leads to a severe lipodystrophic phenotype: new insights into the pathogenicity of nonfarnesylated prelamin-A. , 2011, The Journal of clinical endocrinology and metabolism.

[16]  Y. Jang,et al.  Visceral adiposity and the severity of coronary artery disease in middle-aged subjects with normal waist circumference and its relation with lipocalin-2 and MCP-1. , 2010, Atherosclerosis.

[17]  H. Shapiro,et al.  Inflammation and adipose tissue macrophages in lipodystrophic mice , 2009, Proceedings of the National Academy of Sciences.

[18]  U. Garbin,et al.  The effects of adiponectin on interleukin-6 and MCP-1 secretion in lipopolysaccharide-treated 3T3-L1 adipocytes: role of the NF-kappaB pathway. , 2009, International journal of molecular medicine.

[19]  R. Arora,et al.  The role of adiponectin in obesity, diabetes, and cardiovascular disease. , 2009, Journal of the cardiometabolic syndrome.

[20]  R. Kitazawa,et al.  MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. , 2006, The Journal of clinical investigation.

[21]  C. Kahn,et al.  Critical nodes in signalling pathways: insights into insulin action , 2006, Nature Reviews Molecular Cell Biology.

[22]  J. Pinkney,et al.  Adipokines and the insulin resistance syndrome in familial partial lipodystrophy caused by a mutation in lamin A/C , 2005, Diabetologia.

[23]  R. Yu,et al.  Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-α and IL-6 , 2005 .

[24]  I. S. Wood,et al.  Adipokines: inflammation and the pleiotropic role of white adipose tissue , 2004, British Journal of Nutrition.

[25]  Z. Bloomgarden,et al.  Inflammation and insulin resistance. , 2003, Diabetes care.

[26]  R. Marfella,et al.  Association of low interleukin-10 levels with the metabolic syndrome in obese women. , 2003, The Journal of clinical endocrinology and metabolism.

[27]  B. Miskie,et al.  Elevated Serum C-Reactive Protein and Free Fatty Acids Among Nondiabetic Carriers of Missense Mutations in the Gene Encoding Lamin A/C (LMNA) With Partial Lipodystrophy , 2003, Arteriosclerosis, thrombosis, and vascular biology.

[28]  Y. Matsuzawa,et al.  Serum adiponectin and leptin levels in patients with lipodystrophies , 2002 .

[29]  M. Reitman,et al.  Leptin-replacement therapy for lipodystrophy. , 2002, The New England journal of medicine.

[30]  Y. Terauchi,et al.  The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity , 2001, Nature Medicine.

[31]  S. Gregory,et al.  LMNA, encoding lamin A/C, is mutated in partial lipodystrophy , 2000, Nature Genetics.

[32]  R. Yu,et al.  Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-alpha and IL-6. , 2005, Diabetes research and clinical practice.

[33]  Hilde van der Togt,et al.  Publisher's Note , 2003, J. Netw. Comput. Appl..

[34]  R. Hegele,et al.  Nuclear lamin A/C R482Q mutation in canadian kindreds with Dunnigan-type familial partial lipodystrophy. , 2000, Human molecular genetics.

[35]  J. Field.  Insulin resistance in diabetes. , 1962, Annual review of medicine.