Inherited lipodystrophies and hypertriglyceridemia.

Simha, Vinaya; Garg, Abhimanyu

doi:10.1097/mol.0b013e32832d4a33

Cited by 67Lipid metabolism and disordersLipid metabolism and biosynthesisAdipose Tissue and Metabolism

Inherited lipodystrophies and hypertriglyceridemia.

Simha, Vinaya, Garg, Abhimanyu·2009·Current Opinion in Lipidology

DOI 10.1097/mol.0b013e32832d4a33

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Abstract

PURPOSE OF REVIEW: Inherited lipodystrophies are rare autosomal recessive and dominant disorders characterized by selective, but variable, loss of adipose tissue. Marked hypertriglyceridemia is a common feature of these disorders and highlights the role of adipose tissue in lipid homeostasis. In the last decade, advances have been made in elucidating the molecular basis of many inherited lipodystrophies. We review the new insights in the pathophysiology and treatment of these disorders based on the current understanding of the biologic role of these lipodystrophy genes. RECENT FINDINGS: Eight different genetic loci, including 1-acylglycerol-3-phosphate-O-acyltransferase 2, Berardinelli-Seip congenital lipodystrophy 2, caveolin 1, lamin A/C, peroxisome proliferator-activated receptor gamma, v-AKT murine thymoma oncogene homolog 2, zinc metalloprotease and lipase maturation factor 1 have been described linked to different lipodystrophy syndromes. Mutations in these genes may cause fat loss and dyslipidemia through multiple mechanisms, which remain fully elucidated; however, they may involve defects in development and differentiation of adipocytes, and premature death and apoptosis of adipocytes. Hypertriglyceridemia is a consequence of increased VLDL synthesis from the liver, which is also loaded by ectopic triglyceride deposition, reduced clearance of triglyceride-rich lipoproteins or both. A recent study in mice with Agpat2 deficiency reports marked reduction in serum triglyceride upon feeding a fat-free diet, which suggests that low-fat diets are likely to be beneficial in lipodystrophic patients. Leptin replacement therapy is also a promising therapeutic option for lipodystrophic patients with hypoleptinemia. SUMMARY: Inherited lipodystrophies are an important cause for monogenic hypertriglyceridemia and serve to highlight the role of adipocytes in maintaining normolipidemia.

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Some forms of lipodystrophy manifest at birth, whereas others become evident later in life with loss of fat beginning in childhood and puberty.
“Some forms manifest at birth, whereas others become evident later in life with loss of fat beginning in childhood and puberty (96).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [96]

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Authors: Simha, V., & Garg, A.
Affiliations: The University of Texas Southwestern Medical Center (US)
Corresponding author: Garg, Abhimanyu
ORCID: Simha, Vinaya
Garg, Abhimanyu
Venue: Current Opinion in Lipidology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2009-08
Volume: 20
Issue: 4
Pages: 300-308
ISSN: 0957-9672 (ISSN-L)
DOI: 10.1097/mol.0b013e32832d4a33
OpenAlex: W2004366492
Cited by: 67
References: 64
Citations by year: 2025: 7 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 1 · 2015: 3 · 2014: 4 · 2013: 6 · 2012: 5
FWCI: 1.24
Type: journal article
Language: en
Open access: closed
Locations: Current Opinion in Lipidology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
U.S. Public Health Service (R01-74959)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK054387)
National Center for Research Resources (UL1RR024982)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords: hypertriglyceridemia, adipose tissue loss, adipogenesis, adipocyte apoptosis, dyslipidemia, VLDL synthesis, AGPAT2, caveolin-1, lamin A/C, PPARγ, low-fat diet, leptin replacement therapy, hypoleptinemia, lipid homeostasis
MeSH terms: Animals, Humans, Lipodystrophy, Hypertriglyceridemia, Adipocytes, Lipodystrophy, Congenital Generalized

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