Garg A, Wilson R, Barnes R, Arioglu E, Zaidi Z, Gurakan F, Kocak N, O'Rahilly S, Taylor S I, Patel S B, Bowcock A M
Department of Internal Medicine, and Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas, 75235, USA.
J Clin Endocrinol Metab. 1999 Sep;84(9):3390-4. doi: 10.1210/jcem.84.9.6103.
Congenital generalized lipodystrophy (CGL, Berardinelli-Seip Syndrome, OMIM # 269700) is a rare autosomal recessive disorder characterized by near complete absence of adipose tissue from birth. Affected individuals have marked insulin resistance, hypertriglyceridemia and acanthosis nigricans, and develop diabetes mellitus during teenage years. The genetic defect for CGL is unknown. A semi-automated genome-wide scan with a set of highly polymorphic short tandem repeats (STR) was carried out in 17 well-characterized pedigrees and identified a locus for CGL to chromosome 9q34. The maximum two-point lod score obtained was 3.6 at D9S1818 (theta(max) = 0.05). There was evidence for genetic heterogeneity (alpha = 0.73) and 2 of the pedigrees were unlinked. Multipoint linkage analysis excluding the 2 unlinked families yielded a peak lod score of 5.4 between loci D9S1818 and D9S1826. The CGL1 critical region harbors a plausible candidate gene encoding the retinoid X receptor alpha (RXRA) that plays a central role in adipocyte differentiation. Identification of the CGL gene(s) will contribute to our understanding of the adipocyte differentiation and elucidation of the mechanisms of insulin resistance in disorders of adipose tissue.
先天性全身脂肪营养不良(CGL,贝拉尔迪内利-塞普综合征,OMIM #269700)是一种罕见的常染色体隐性疾病,其特征是出生时几乎完全没有脂肪组织。受影响的个体有明显的胰岛素抵抗、高甘油三酯血症和黑棘皮症,并在青少年时期发展为糖尿病。CGL的基因缺陷尚不清楚。我们对17个特征明确的家系进行了一组高度多态性短串联重复序列(STR)的半自动全基因组扫描,并确定了CGL在9号染色体q34上的一个位点。在D9S1818处获得的最大两点连锁值为3.6(θ(max)=0.05)。有证据表明存在遗传异质性(α=0.73),其中2个家系未连锁。排除这2个未连锁家族后的多点连锁分析在D9S1818和D9S1826位点之间产生了5.4的最高连锁值。CGL1关键区域包含一个可能的候选基因,该基因编码视黄酸X受体α(RXRA),其在脂肪细胞分化中起核心作用。CGL基因的鉴定将有助于我们理解脂肪细胞分化,并阐明脂肪组织疾病中胰岛素抵抗的机制。