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1 MAD associated with progeroid appearance and generalized lipodystrophy.
2  pathway, and its mutations cause congenital generalized lipodystrophy.
3 y to lipoatrophy such as in individuals with generalized lipodystrophy.
4  junctions; the absence of seipin results in generalized lipodystrophy.
5 f adipose tissue in the most severe forms of generalized lipodystrophy.
6 dherent skin, an aged appearance, and severe generalized lipodystrophy.
7 riched in a subset of patients with acquired generalized lipodystrophy (17 of 46 [37%]), particularly
8                     Ten patients with either generalized lipodystrophy (8 patients) or Dunnigan's par
9          Leptin is an approved treatment for generalized lipodystrophy, a condition associated with s
10                                     Acquired generalized lipodystrophy (AGL) is a rare condition char
11 ient with the unique combination of acquired generalized lipodystrophy and Crohn's disease (AGLCD) fe
12 versal feature of human and rodent models of generalized lipodystrophy and is also a common feature o
13 hat mutations in AGPAT2 may cause congenital generalized lipodystrophy by inhibiting triacylglycerol
14   Seipin deficiency causes severe congenital generalized lipodystrophy (CGL) and metabolic disease.
15                                   Congenital generalized lipodystrophy (CGL) is a rare autosomal rece
16                                   Congenital generalized lipodystrophy (CGL) is a rare disorder chara
17 e exhibit many of the features of congenital generalized lipodystrophy (CGL), an autosomal recessive
18                                   Congenital generalized lipodystrophy (CGL), secondary to AGPAT2 mut
19 fied in individuals affected with congenital generalized lipodystrophy (CGL).
20 exhibit a syndrome that resembles congenital generalized lipodystrophy in humans.
21                                   Congenital generalized lipodystrophy is an autosomal recessive diso
22  of such disorders of liporegulation include generalized lipodystrophies, mutations of leptin and lep
23 observed either from birth, as in congenital generalized lipodystrophy, or later in life, as in famil
24                          In a mouse model of generalized lipodystrophy, REGN4461 alleviated hyperphag
25 ibited MSTN signaling in a diabetic model of generalized lipodystrophy to analyze its effects on gluc
26 d cMAT are preserved in mice with congenital generalized lipodystrophy type 3.
27  Loss of rMAT occurs in mice with congenital generalized lipodystrophy type 4, whereas both rMAT and