Dysadipocytokinemia in Werner Syndrome and Its Recovery by Treatment With Pioglitazone
- Koutaro Yokote, MD12,
- Kazuo Hara, MD3,
- Seijiro Mori, MD12,
- Takashi Kadowaki, MD3,
- Yasushi Saito, MD12 and
- Makoto Goto, MD45
- 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Chiba University Hospital, Chiba City, Japan
- 2Department of Clinical Cell Biology, Chiba University Graduate School of Medicine, Chiba City, Japan
- 3Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
- 4Department of Rheumatology, Tokyo Metropolitan Otsuka Hospital, Tokyo, Japan
- 5Institute of Bioengineering, Toin Yokohama University, Yokohama, Japan
- Address correspondence to Koutaro Yokote, MD, Division of Endocrinology and Metabolism, Department of Internal Medicine, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. E-mail: kyokote-cib{at}umin.ac.jp
Werner syndrome (WS) (Mendelian Inheritance in Man no. 277700) is an autosomal recessive disorder known for progeroid phenotypes including graying and loss of hair, juvenile cataracts, insulin-resistant diabetes, skin atrophy, premature atherosclerosis, and cancer (1). Mutations in WRN, a RECQ family DNA/RNA helicase gene, have been identified to cause this disease. The mechanism for insulin resistance in WS remains to be elucidated.
Adipocytes secrete a number of hormones (or adipocytokines), such as tumor necrosis factor-α (TNF-α), leptin, adiponectin, and resistin, thereby regulating insulin sensitivity (2). WS patients typically show the lipoatrophic skinny extremities with an obese trunk (1). The accumulated intra-abdominal visceral fat (3) suggests an altered production of adipocytokines.
To investigate the role of adipocytokines in the pathophysiology of WS, we …
