Ebihara Ken, Kusakabe Toru, Masuzaki Hiroaki, Kobayashi Nozomi, Tanaka Tomohiro, Chusho Hideki, Miyanaga Fumiko, Miyazawa Takashi, Hayashi Tatsuya, Hosoda Kiminori, Ogawa Yoshihiro, Nakao Kazuwa
Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan.
J Clin Endocrinol Metab. 2004 May;89(5):2360-4. doi: 10.1210/jc.2003-031211.
Congenital generalized lipodystrophy (CGL), Berardinelli-Seip syndrome, is a rare metabolic disorder characterized by a near total lack of adipose tissue from birth or early infancy. Recently, seipin, encoding a 398-amino acid protein of unknown function, and AGPAT2, encoding 1-acyl-sn-glycerol-3-phosphate acyltransferase 2, were identified as causative genes for CGL. Seipin mutations were found in patients from families originating from Europe and the Middle East. AGPAT2 mutations were found predominantly in African ancestry. However, no information is available on these genes in the pathogenesis of CGL in Asian ancestry. We examined the sequences of the entire coding region of seipin and AGPAT2 in four Japanese CGL patients from independent families. Their average body fat content was 4.7 +/- 0.5%, and the plasma leptin level was 1.15 +/- 0.14 ng/ml. We identified a novel nonsense mutation of seipin at codon 275 (R275X). Of four CGL patients, three were homozygous for R275X. No seipin mutation was found in any exon in one patient. We did not find any AGPAT2 mutations in our Japanese patients, suggesting that AGPAT2 is a minor causative gene, if any, for CGL in Japanese. This is the first report on gene and phenotype analysis of CGL in Japanese.
先天性全身脂肪营养不良(CGL),即贝拉尔迪内利 - 塞普综合征,是一种罕见的代谢紊乱疾病,其特征是自出生或婴儿早期就几乎完全缺乏脂肪组织。最近,编码一种功能未知的398个氨基酸蛋白质的丝蛋白(seipin)和编码1 - 酰基 - sn - 甘油 - 3 - 磷酸酰基转移酶2的AGPAT2被确定为CGL的致病基因。在来自欧洲和中东的家族患者中发现了丝蛋白突变。AGPAT2突变主要在非洲血统人群中发现。然而,关于这些基因在亚洲血统CGL发病机制中的信息尚无报道。我们检测了来自独立家族的4名日本CGL患者丝蛋白和AGPAT2整个编码区的序列。他们的平均体脂含量为4.7±0.5%,血浆瘦素水平为1.15±0.14 ng/ml。我们在丝蛋白的第275密码子处鉴定出一个新的无义突变(R275X)。在4名CGL患者中,3名是R275X纯合子。在1名患者的任何外显子中均未发现丝蛋白突变。在我们的日本患者中未发现任何AGPAT2突变,这表明AGPAT2即使是CGL在日本人中的致病基因,也是次要的。这是关于日本CGL基因和表型分析的首次报道。