จำนวน 15 ความเห็น, หน้า่ | -1-

ความเห็นเพิ่มเติมที่ 3 12 ก.ค. 2547 (21:07)
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ความเห็นเพิ่มเติมที่ 4 13 ก.ค. 2547 (06:17)
Lipodystrophies are clinically heterogeneous acquired or inherited disorders characterized by the selective loss of adipose tissue. Affected patients are predisposed to insulin resistance and its attendant complications, including diabetes mellitus, dyslipidemia, hepatic steatosis, and acanthosis nigricans. Features of polycystic ovary syndrome — hirsutism, oligoamenorrhea, and polycystic ovaries — may develop in affected women. The mechanisms involved in the pathogenesis of various types of lipodystrophy are prostulated.

More than a century after the clinical phenotype was first described, we are beginning to understand the molecular and cellular mechanisms underlying lipodystrophies. The genetic basis of many inherited lipodystrophy syndromes has been elucidated through the systematic characterization of phenotypes based on distinct clinical features and unique patterns of adipose-tissue distribution, together with techniques derived from research in molecular biology and sequencing of the human genome. This review focuses on the clinical features, underlying pathogenetic mechanisms, and management of various types of lipodystrophy.


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ความเห็นเพิ่มเติมที่ 5 13 ก.ค. 2547 (06:24)
Acquired Lipodystrophies

Acquired lipodystrophies are more common than the inherited varieties and are discussed first. Each acquired lipodystrophy has a unique clinical picture and underlying pathogenic mechanism.

Lipodystrophy in Patients with Human Immunodeficiency Virus Infection

Clinical Picture - Lipodystrophy characterized by the loss of subcutaneous fat from the face, arms, and legs has been reported to develop in patients infected with the human immunodeficiency virus (HIV) who are receiving highly active antiretroviral therapy that includes protease inhibitors. Some HIV-infected patients with lipodystrophy may have concomitant deposition of excess fat in the neck and upper back, causing a double chin and a buffalo hump, respectively, and in the trunk. Approximately 1 million people in the United States are infected with HIV, and about 42 million are infected worldwide. In developed countries approximately half of HIV-infected persons receive antiretroviral therapy, and more than half of those take protease inhibitors. Lipodystrophy develops in approximately 40 percent of patients who are treated with a protease inhibitor for longer than one year. Thus, acquired lipodystrophy in HIV-infected patients is by far the most prevalent type of lipodystrophy, with more than 100,000 such patients in the United States.

Pathogenetic Basis - Though the mechanisms by which protease inhibitors cause lipodystrophy remain unknown, there are interesting possibilities. Several protease inhibitors impair the differentiation of preadipocytes, and mild-to-moderate apoptosis of subcutaneous adipocytes was reported in biopsy specimens from the leg in 10 of 13 patients with lipodystrophy who were receiving a regimen containing protease inhibitors. Adipose tissue from patients with lipodystrophy who are receiving protease inhibitors has reduced messenger RNA (mRNA) expression of several key transcription factors involved in adipogenesis, including sterol regulatory element–binding protein 1c (SREBP1c) and peroxisome-proliferator–activated receptor (PPAR). However, although the expression of PPAR protein was reduced, that of SREBP1c protein was increased. Interestingly, additional experimental data in transgenic mice support these findings: the overexpression of SREBP1c induces lipodystrophy. In humans, reduced PPAR activity owing to inactivating mutations causes familial partial lipodystrophy.


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ความเห็นเพิ่มเติมที่ 6 13 ก.ค. 2547 (06:27)
Acquired Partial Lipodystrophy (The Barraquer–Simons Syndrome)

Clinical Picture - Before the recognition of lipodystrophy in HIV-infected persons, acquired partial lipodystrophy, originally described by Mitchell, Barraquer, and Simons, was the most common acquired lipodystrophy. Nevertheless, it is rare — approximately 250 patients of various ethnic origins have been described. The male-to-female ratio is approximately 1:4. The fat loss occurs during childhood or adolescence, affecting the face, neck, arms, thorax, and upper abdomen in a cephalocaudal fashion. In contrast, excess fat may be deposited in the hips and legs, particularly in affected women. Insulin resistance and its accompanying complications appear to be infrequent in this syndrome. In approximately 20 percent of the patients, mesangiocapillary (membranoproliferative) glomerulonephritis developed about eight years after the onset of lipodystrophy. Other autoimmune diseases, including systemic lupus erythematosus and juvenile dermatomyositis, have also developed in a few of these patients.

Pathogenetic Basis - Almost all patients with acquired partial lipodystrophy have low levels of serum C3 accompanied by detectable levels of a circulating polyclonal IgG called C3 nephritic factor. Levels of other complement factors are normal. C3 nephritic factor stabilizes the enzyme C3 convertase (C3b,Bb), which splits C3, causing unopposed activation of the alternative complement pathway and excessive consumption of C3. The synthesis of C3b,Bb also involves factor D (adipsin), which is produced mainly by adipocytes. C3 nephritic factor–induced lysis of adipocytes that express factor D may be involved in the pathogenesis of this form of lipodystrophy. However, why adipose tissue in the legs is spared and whether autoimmunity is triggered by viral or other infections remain unclear.


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ความเห็นเพิ่มเติมที่ 7 13 ก.ค. 2547 (06:33)
Acquired Generalized Lipodystrophy

Clinical Picture - Acquired generalized lipodystrophy has been reported in approximately 80 patients, most of whom were white (male-to-female ratio, 1:3). The fat loss typically occurs during childhood and adolescence, affecting large areas of the body, particularly the face, arms, and legs. Subcutaneous fat may also be lost from the palms and soles, while retroorbital and bone marrow fat are preserved. The degree of loss of intraabdominal fat varies. Affected children may have a voracious appetite. Acanthosis nigricans and hepatic steatosis also develop in most patients beginning in childhood. Cirrhosis has been reported in about one fifth of the patients as a late sequela of hepatic steatosis or autoimmune hepatitis. Most patients have low serum levels of leptin and adiponectin.

Pathogenetic Basis - The onset of acquired generalized lipodystrophy has been heralded by an episode of subcutaneous inflammatory nodules, termed panniculitis, in approximately 25 percent of patients. A hallmark of these lesions is the infiltration of adipose tissue with histiocytes, lymphocytes, and multinucleated giant cells, together with a granulomatous reaction. Initially, these lesions heal, with localized loss of subcutaneous fat, but subsequently fat is lost from almost all subcutaneous regions, eventually causing generalized lipodystrophy. Another 25 percent of affected patients have associated autoimmune diseases, particularly juvenile dermatomyositis. However, roughly half the patients with acquired generalized lipodystrophy have the idiopathic variety, which involves neither associated panniculitis nor autoimmune diseases. Patients in whom panniculitis is the initial event have less severe fat loss and a lower prevalence of diabetes and hypertriglyceridemia than do patients with the other varieties. In patients with antecedent panniculitis and concomitant autoimmune diseases, the loss of adipose tissue is presumed to be immune mediated, but other mechanisms are probably involved in the idiopathic variety.


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ความเห็นเพิ่มเติมที่ 8 13 ก.ค. 2547 (06:35)
Localized Lipodystrophies

Most people with localized lipodystrophies lose subcutaneous fat from small areas, leaving indentations. In some, large regions of the trunk or limbs may be involved. The cause of such localized fat loss varies and may be related to injected drugs such as insulin and corticosteroids, recurrent pressure, panniculitis, or unknown mechanisms.

An unusual centrifugally spreading variety affecting abdominal fat in young children has been reported in Japan, Korea, and Singapore; spontaneous recovery after several years has been observed in over half the patients.


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ความเห็นเพิ่มเติมที่ 9 13 ก.ค. 2547 (06:40)
Congenital Generalized Lipodystrophy (The Berardinelli–Seip Syndrome)

Molecular Basis of Congenital Generalized Lipodystrophy Type 1

Two molecularly distinct forms of congenital generalized lipodystrophy have been defined — type 1 and type 2. Some patients have neither type, so that additional genes are most likely involved.

Positional cloning was used to identify the aberrant gene — 1-acylglycerol-3-phosphate O-acyltransferase 2 (AGPAT2) — in patients from several pedigrees in which the lipodystrophy was linked to chromosome 9q34. Several homozygous or compound heterozygous mutations in the AGPAT2 gene were found in affected patients. Interestingly, almost all patients of African origin have a splice-site mutation (IVS4-2A>G) on the same haplotype, suggesting that the mutation has a common ancestral origin.

The five known isoforms of AGPAT catalyze an acylation reaction at the stereospecific number-2 position of glycerol-3-phosphate during the synthesis of triglycerides and phospholipids. AGPAT2 mRNA expression is at least twice as high as that of AGPAT1 in human omental adipose tissue but is lower in the liver and far lower in the skeletal muscle. These observations suggest that the aberrant AGPAT2 enzyme may cause lipodystrophy by reducing the synthesis of triglycerides in adipose tissue, thus leading to adipocytes that are depleted of triglycerides, or by reducing the bioavailability of phosphatidic acid and phospholipids that are important for intracellular signaling and membrane functions. Affected patients lack metabolically active adipose tissue in most subcutaneous areas, intraabdominal and intrathoracic regions, and bone marrow, whereas mechanical adipose tissue, which fulfills a protective and cushioning function, such as in the joints, orbits, palms and soles, scalp, perineum, vulva, and pericalyceal regions of the kidneys, appears to be spared. The preservation of mechanical adipose tissue in patients with AGPAT2 mutations may be due to the increased expression of other AGPAT isoforms in these adipose-tissue depots.

Molecular Basis of Congenital Generalized Lipodystrophy Type 2

Magre and colleagues reported mutations in the seipin gene in patients from several large consanguineous pedigrees from Lebanon and Norway in which linkage to chromosome 11q13 had been noted. The seipin gene encodes a 398–amino-acid protein of unknown function; thus, the mechanisms causing lipodystrophy remain unclear. However, the fact that affected patients have high levels of expression of seipin mRNA in the brain yet weak expression in adipose tissue suggests that the central nervous system is involved. Patients with seipin mutations have a higher prevalence of mild mental retardation and hypertrophic cardiomyopathy than do those with AGPAT2 mutations. Type 2 patients lack both metabolically active and mechanical adipose tissue.

Other Types of Congenital Generalized Lipodystrophy

Some patients with congenital generalized lipodystrophy (less than 20 percent) have neither mutations nor linkage to either the AGPAT2 or seipin gene, suggesting that additional loci and other distinct pathways are involved.


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ความเห็นเพิ่มเติมที่ 10 13 ก.ค. 2547 (06:45)
Dunnigan Variety of Familial Partial Lipodystrophy

The identification of a locus for the Dunnigan variety of familial partial lipodystrophy, on chromosome 1q21 [PDB] –22, led to the identification of a missense mutation in the gene encoding lamins A and C (LMNA) in affected members of a Canadian pedigree. Subsequently, many more missense LMNA mutations have been reported.

Lamins belong to the intermediate filament family of proteins that compose the nuclear lamina — a polymeric structure intercalated between chromatin and the inner nuclear membrane. The LMNA gene contains 12 exons and encodes lamins A and C by alternative splicing within exon 10. Lamins provide structural integrity to the nuclear envelope and associate with chromatin and several other nuclear proteins.

Loss of adipocytes associated with LMNA mutations are most likely due to a disruption of nuclear function resulting in cell death or to a disruption of the interaction between lamins and transcription factors such as SREBP1c. Fibroblasts from patients with the Dunnigan variety of familial partial lipodystrophy have abnormal nuclear blebbing and disorganized nuclear lamina meshwork. The mechanisms underlying the regional differences in fat loss, however, remain unclear, since no differences in the expression of lamins A and C were noted in adipocytes from the omentum and subcutaneous abdominal and neck regions.

The site of missense mutations influences the phenotype. Approximately three fourths of patients have mutations substituting glutamine, leucine, or tryptophan for the arginine residue at position 482. In a few of these patients, mild myopathy, muscular dystrophies, cardiomyopathy, and conduction-system disturbances such as atrial fibrillation requiring the implantation of a pacemaker, also develop, leading to the hypothesis that LMNA mutations cause a multisystem dystrophy syndrome in which the severity and age at onset of various clinical manifestations may differ depending on the site of mutations. The interaction of certain domains of lamins A and C with other nuclear-envelope proteins with tissue-restricted expression may confer tissue-specific abnormalities.


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ความเห็นเพิ่มเติมที่ 11 13 ก.ค. 2547 (06:50)
Familial Partial Lipodystrophy Associated with PPAR Gene Mutations

Recently, my colleague and I described a heterozygous missense mutation — Arg397Cys — in the PPAR gene in a 64-year-old woman with diabetes, hypertriglyceridemia, hypertension, hirsutism, and marked loss of subcutaneous fat from her arms, legs, and face. Her fat loss was more prominent in her forearms and calves than in her upper arms and thighs. Her truncal region was spared, and no excess fat was noted in her neck. Subsequently, three persons with insulin resistance, diabetes, hypertension, hypertriglyceridemia, and a heterozygous mutation in the PPAR gene (either Pro467Leu or Val290Met) were recognized to have familial partial lipodystrophy. Recently, another missense mutation, Phe388Leu, has been associated with familial partial lipodystrophy. The age at onset and pattern of progression of fat loss associated with this type of lipodystrophy remain unclear.

The PPAR protein is a ligand-inducible nuclear transcription factor expressed at high levels in adipose tissue that has an essential role in adipogenesis. The Arg397Cys mutation is predicted to disrupt the formation of a salt bridge between arginine at position 397 and glutamic acid at position 324. The other three mutant PPAR proteins were found to be transcriptionally impaired, had reduced ligand binding, and inhibited the action of coexpressed wild-type PPAR in a dominant negative manner. Thus, although mutations in the PPAR gene may cause lipodystrophy by inhibiting the differentiation of adipocytes, the reasons for the isolated loss of peripheral subcutaneous fat remain unclear.


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ความเห็นเพิ่มเติมที่ 12 14 ก.ค. 2547 (09:39)
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