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1 nt in LMNA associated with Dunnigan familial partial lipodystrophy.
2  We describe a family with MPGN and acquired partial lipodystrophy.
3 utaneous fat have a phenotype reminiscent of partial lipodystrophy.
4  chylomicronemia syndrome (FCS); or familial partial lipodystrophy.
5 odystrophy, or later in life, as in familial partial lipodystrophy.
6 C has been reported in patients with MAD and partial lipodystrophy.
7 ted AKT activation in metabolic tissues, and partial lipodystrophy.
8 h increased hepatic RIPK3 levels in familial partial lipodystrophy.
9 rfism, mandibular hypoplasia, hyperopia, and partial lipodystrophy.
10 with NAFLD and in PLIN1 -associated familial partial lipodystrophy.
11 zed lipodystrophy (8 patients) or Dunnigan's partial lipodystrophy (2 patients) were included in this
12  gene (encoding lamin A/C) underlie familial partial lipodystrophy, a syndrome of monogenic insulin r
13 ntial splice site mutation in a proband with partial lipodystrophy and a history of childhood yolk sa
14  treatment of a single patient with atypical partial lipodystrophy and a history of undetectable lept
15 ty liver dystrophy (fld) mice, which exhibit partial lipodystrophy and have diminished peripheral adi
16 ociated with adverse side effects, including partial lipodystrophy and metabolic syndrome.
17 essed in adipose tissue and causal genes for partial lipodystrophies, and evidence of sex-dimorphism.
18 - a disorder characterized by short stature, partial lipodystrophy, and insulin resistance.
19 rticular muscular dystrophy, cardiomyopathy, partial lipodystrophy, and progeroid syndromes.
20 ncluding muscular dystrophy, cardiomyopathy, partial lipodystrophy, and progeroid syndromes.
21 bited a reduction in body weight and length, partial lipodystrophy, and systemic insulin resistance.
22 lear LMNA cause laminopathies, which include partial lipodystrophies associated with metabolic syndro
23 bjects; 2) describe a stereotyped pattern of partial lipodystrophy associated with all the features o
24 ism and estimating the pathogenesis of human partial lipodystrophy caused by CIDEC mutations.
25 in patients with a novel subtype of familial partial lipodystrophy, designated as FPLD4.
26                                     Familial partial lipodystrophy, Dunnigan variety, (FPLD, OMIM 308
27 m an undiagnosed autosomal dominant familial partial lipodystrophy (FPL) pedigree and identified only
28                                     Familial partial lipodystrophy (FPLD) is a heterogenous group of
29                                     Familial partial lipodystrophy (FPLD), Dunnigan variety, is an au
30 olve muscle defects, and the other, familial partial lipodystrophy (FPLD), involves loss of subcutane
31 udes residues genetically linked to familial partial lipodystrophy (FPLD).
32 uscular dystrophy and Dunnigan-type familial partial lipodystrophy (FPLD).
33 ith forms of muscular dystrophy and familial partial lipodystrophy (FPLD).
34 dystrophy syndrome similar to human familial partial lipodystrophy FPLD2, with profound insulin resis
35 ects in some ultra-rare subtypes of familial partial lipodystrophies (FPLs) remain unidentified.
36                                 The apparent partial lipodystrophy in Reep1 null mice, although less
37                                              Partial lipodystrophy is an underdiagnosed condition.
38 g genetic studies have suggested that subtle partial lipodystrophy is likely to be a major factor in
39 or was shown in family members with acquired partial lipodystrophy, it did not segregate with the ren
40                                              Partial lipodystrophy (PLD; MIM 151660) is an inherited
41 egregated with a similar phenotype including partial lipodystrophy, severe insulin resistance and typ
42 btle redistribution in some individuals with partial lipodystrophy to a near-complete absence of adip
43 we show a polygenic contribution to familial partial lipodystrophy type 1, a severe form of insulin r
44 l recessive mutations in Lmna cause familial partial lipodystrophy type 2 (FPLD2) are poorly understo
45 e development or function or, in the case of partial lipodystrophy, why only some adipose depots shou