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Lipodystrophy for the Diabetologist—What to Look For

  • Pathogenesis of Type 2 Diabetes and Insulin Resistance (M-E Patti, Section Editor)
  • Published:
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Abstract

Purpose of Review

Genetic or acquired lipodystrophies are characterized by selective loss of body fat along with predisposition towards metabolic complications of insulin resistance, such as diabetes mellitus, hypertriglyceridemia, hepatic steatosis, polycystic ovarian syndrome, and acanthosis nigricans. In this review, we discuss the various subtypes and when to suspect and how to diagnose lipodystrophy.

Recent Findings

The four major subtypes are autosomal recessive, congenital generalized lipodystrophy (CGL); acquired generalized lipodystrophy (AGL), mostly an autoimmune disorder; autosomal dominant or recessive familial partial lipodystrophy (FPLD); and acquired partial lipodystrophy (APL), an autoimmune disorder. Diagnosis of lipodystrophy is mainly based upon physical examination findings of loss of body fat and can be supported by body composition analysis by skinfold measurements, dual-energy x-ray absorptiometry, and whole-body magnetic resonance imaging. Confirmatory genetic testing is helpful in the proband and at-risk family members with suspected genetic lipodystrophies. The treatment is directed towards the specific comorbidities and metabolic complications, and there is no treatment to reverse body fat loss. Metreleptin should be considered as the first-line therapy for metabolic complications in patients with generalized lipodystrophy and for prevention of comorbidities in children. Metformin and insulin therapy are the best options for treating hyperglycemia and fibrates and/or fish oil for hypertriglyceridemia.

Summary

Lipodystrophy should be suspected in lean and muscular subjects presenting with diabetes mellitus, hypertriglyceridemia, non-alcoholic fatty liver disease, polycystic ovarian syndrome, or amenorrhea. Diabetologists should be aware of lipodystrophies and consider genetic varieties as an important subtype of monogenic diabetes.

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Acknowledgments

We thank Tea Huseinbegovic, B.S., for help with the illustration.

Funding

A.G. and N.P are supported by the National Institutes of Health grant R01-DK105448 and A.G. is also supported by the Southwestern Medical Foundation.

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Authors and Affiliations

  1. Division of Pediatric Endocrinology, Department of Pediatrics, UT Southwestern Medical Center, Dallas, TX, USA

    Nivedita Patni

  2. Division of Nutrition and Metabolic Diseases, Department of Internal Medicine and the Center for Human Nutrition, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390-8537, USA

    Abhimanyu Garg

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  1. Nivedita Patni
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Correspondence to Abhimanyu Garg.

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N.P. have no financial or non-financial interests that are directly or indirectly related to the work submitted for publication. A.G. consults for Amryt Pharma PLC and Regeneron and has received grant support from Amryt Pharma PLC, Regeneron, Quintiles, Akcea Pharmaceuticals, and Intercept Pharmaceuticals. A.G. is coholder of a patent for “use of leptin for treating human lipoatrophy and a method of determining predisposition to said treatment” but receives no financial compensation.

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Patni, N., Garg, A. Lipodystrophy for the Diabetologist—What to Look For. Curr Diab Rep 22, 461–470 (2022). https://doi.org/10.1007/s11892-022-01485-w

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