Last updated:
12/23/2025
Years published: 1988, 1989, 1992, 1998, 2003, 2004, 2012, 2015, 2025
NORD gratefully acknowledges Abhimanyu Garg, MD, Professor of Internal Medicine, Chief, Section of Nutrition and Metabolic Diseases, Distinguished Chair in Human Nutrition Research, UT Southwestern Medical Center at Dallas, and Gioconda Alyea, MD (FMG), MS, National Organization for Rare Disorders, for the preparation of this report.
Summary
Acquired lipodystrophy is a general term for types of lipodystrophy that are not inherited but rather acquired at some point during life.
Acquired lipodystrophies do not have a direct genetic cause, but rather many different factors may be involved. Acquired lipodystrophies can be caused by medications, autoimmunity or for unknown reasons (idiopathic).
Subtypes of acquired lipodystrophy include acquired generalized lipodystrophy (Lawrence syndrome), acquired partial lipodystrophy (Barraquer-Simons syndrome), localized lipodystrophy and high active antiretroviral induced lipodystrophy, which may develop in HIV-infected individuals undergoing a specific form of treatment. Onset of acquired forms of lipodystrophy can occur during childhood, adolescence or adulthood. Affected individuals develop characteristic loss of body fat (adipose tissue) affecting specific areas of the body, especially the arms, legs, face, neck and chest or thoracic regions. In some people, metabolic complications associated with insulin resistance can develop. Such complications include an inability to break down glucose (glucose intolerance), elevated levels of triglycerides (a type of fat) in the blood (hypertriglyceridemia) and diabetes. Additional symptoms such as fat accumulation in the liver (fatty liver or hepatic steatosis) may also occur.
Introduction
Lipodystrophy is a general term for a group of disorders that are characterized by complete (generalized) or partial loss of adipose tissue. Some forms of lipodystrophy are acquired, and others are genetic. The degree of severity and the specific areas of the body affected can vary among the lipodystrophies. Some doctors refer to the loss of adipose tissue that characterizes these disorders as lipoatrophy rather than lipodystrophy.
Acquired lipodystrophy encompasses several subtypes. The specific symptoms, severity and prognosis can vary greatly depending upon the specific type of acquired lipodystrophy. The specific symptoms and severity can also vary among individuals with the same subtype. It is important to note that affected individuals will not have all the symptoms discussed below. Affected individuals should talk to their doctor and medical team about their specific case, associated symptoms and overall prognosis.
Acquired generalized lipodystrophy (AGL; Lawrence syndrome)
People with this form of lipodystrophy have a loss of subcutaneous fat from the face, neck, and arms and legs. The overall extent and pattern of fat loss in AGL is highly variable and can differ significantly from one person to another. In some people, fat may also be lost from the palms of the hands and the soles of the feet. Intra-abdominal fat may be lost in some people but preserved in others. The loss of bone marrow fat rarely occurs. Fat loss associated with AGL may occur rapidly over a few weeks or slowly over several months or even years. Fat loss can be severe. Eventually, generalized and near complete loss of fat may occur resulting in prominent veins that bulge out from underneath the skin and an overall muscular appearance.
AGL usually develops during childhood or adolescence but can occur at any age. During childhood, affected individuals are described as being voracious eaters and may have accelerated growth. Affected individuals may also experience fatigue.
Individuals with AGL often develop severe insulin resistance, which can result in a variety of metabolic complications. Affected individuals may develop acanthosis nigricans, a skin condition characterized by abnormally increased coloration (hyperpigmentation) and “velvety” thickening (hyperkeratosis) of the skin, particularly of skin fold regions, such as of the neck and groin and under the arms (axillae). Other complications of insulin resistance may occur including glucose intolerance, hypertriglyceridemia and diabetes. These symptoms are often very difficult to control, and diabetes is often severe. Diabetes often occurs after the development of lipodystrophy but in some people may occur almost simultaneously.
Some individuals develop abnormal enlargement of the liver (hepatomegaly) due to the infiltration and accumulation of fat within the liver. This can be known as hepatic steatosis or fatty liver. Fatty accumulation of the liver in individuals with AGL is often severe and can cause damage and scarring (cirrhosis) to the liver and, eventually, liver dysfunction. In some people, liver enlargement may be due to autoimmune hepatitis. However, the diagnosis of autoimmune hepatitis should be made after review by expert pathologists.
Some individuals may have extreme hypertriglyceridemia and chylomicronemia, a condition characterized by the accumulation of fatty droplets called chylomicrons in the plasma. In some people, this can result in episodes of acute inflammation of the pancreas (pancreatitis). Pancreatitis can be associated with abdominal pain, chills, jaundice, weakness, sweating, vomiting and weight loss.
After puberty, some females with AGL may develop polycystic ovary syndrome (PCOS). PCOS is characterized by an imbalance of sex hormones. Affected females have too much androgen, a male hormone, in the body. PCOS can result in irregular menstrual periods or a lack of menstruation, oily skin that is prone to acne, cysts on the ovaries and a male pattern of hair growth (mild hirsutism). Hair may develop on the upper lip and chin.
AGL can be subdivided into three separate subtypes known as:
Individuals with panniculitis-associated AGL generally have a less severe form of the disorder. Panniculitis is inflammation of subcutaneous fat. Individuals with panniculitis-associated AGL may have less severe fat loss and metabolic complications. Fat loss in panniculitis-associated AGL may be localized to a specific part of the body. Lipodystrophy in panniculitis-associated AGL is preceded by the development of painful subcutaneous nodules or lesions consisting of small spots or bumps (maculopapular lesions).
Individuals with autoimmune-associated AGL have past or present evidence of an autoimmune disorder in addition to lipodystrophy. In these people, AGL is thought to be caused by underlying autoimmune abnormalities. Autoimmune disorders that have been associated with AGL include juvenile dermatomyositis, Sjogren’s syndrome and rheumatoid arthritis.
In the third type of AGL, panniculitis and autoimmune disorders do not occur, and the underlying cause is unknown (idiopathic).
Recently, development of autoantibodies (an autoantibody is an immune protein that mistakenly targets and damages healthy tissue) to perilipin 1 (PLIN1) protein have been discovered in about one third of the people with AGL, especially in those who have panniculitis subtype of AGL. These antibodies may merely be a marker of lipodystrophy in patients with AGL or may be causing lipodystrophy (fat loss due to autoimmune destruction of adipocytes).
Acquired partial lipodystrophy (APL; Barraquer-Simons syndrome)
This form of acquired lipodystrophy usually has onset during childhood. Fat distribution is normal at birth and during early childhood. However, at some point later during childhood or adolescence, affected individuals lose subcutaneous fat from the face. Most individuals have noticeable fat loss by the age of 13. Eventually, fat loss extends to the arms, neck, chest and sometimes the upper abdomen. The legs, hips and gluteal regions are usually spared. After puberty in some females, these areas may have disproportionately excess fat accumulation in the hips and legs. Fat loss is often gradual and may occur over a few months to several years.
Approximately 8% of individuals with APL eventually develop a kidney disorder known as membranoproliferative glomerulonephritis, which is characterized by inflammation and degeneration of the tiny clusters of blood vessels (capillaries) in the special structures called renal glomeruli that filter the blood as it passes through the kidneys. Glomerulonephritis results in an impaired ability to remove waste and fluid products from the body which then build up in the blood stream. Kidney problems can develop including blood in the urine, dark urine, decreased urine output and swelling of various parts of the body. Potentially, kidney disease can progress so that the kidneys fail to function adequately (renal failure or insufficiency). Membranoproliferative glomerulonephritis specifically refers to when the condition is caused by an abnormal immune system response.
As they age, some affected individuals may develop abnormally accumulation of yellow or white extracellular material (drusen) in the retina, a membrane in the back of the eyes. Some older people may develop macular degeneration. Macular degeneration is a general term for a group of eye disorders characterized by the deterioration of the oval-shaped yellow spot (macula) near the center of the retina. The macula is essential for proper vision when looking straight ahead (central vision) and with seeing fine details.
Fifteen percent of patients with APL have associated autoimmune disorders including lupus, dermatomyositis, Celiac disease, pernicious anemia and vasculitis. Abnormal enlargement of liver (hepatomegaly) has been reported in some people.
Most forms of lipodystrophy are associated with metabolic complications due to insulin resistance. Even in patients with APL, 38% had either diabetes mellitus or glucose intolerance, 43% had hypertriglyceridemia and 61% had fatty liver or metabolic dysfunction-associated steatohepatitis (MASH).
High active antiretroviral therapy (HAART) induced lipodystrophy (LD-HIV)
This form of lipodystrophy occurs in individuals with human immunodeficiency virus (HIV) after receiving antiretroviral therapy known as HIV-1 protease inhibitor-containing HAART. The development of lipodystrophy is related to the intensity and duration of treatment. In many people, protease inhibitors and nucleoside reverse transcriptase inhibitors are implicated in the development of lipodystrophy. In most people, LD-HIV develops in individuals who have received this therapy for two years or more.
Most people gradually lose subcutaneous fat from the arms, legs and face. Some people may develop excess fat in the face, neck, upper back and waist. This can cause a double chin, a hump on the upper back and expand the circumference of the waist. Fat loss gets progressively worse with ongoing HAART therapy and does not reverse when the therapy is discontinued. Many people also develop hypertriglyceridemia. Diabetes may also occur but is rare. These patients may be at an increased risk of developing coronary heart disease.
Current regimens for treating HIV-infected patients do not include HIV-protease inhibitors and therefore, the prevalence of lipodystrophy among HIV-infected patients is much lower than before.
Localized lipodystrophy
This form of lipodystrophy is characterized by subcutaneous fat loss in a small area of the body only. It includes several subtypes:
Acquired lipodystrophies can be caused by medications, autoimmune reactions or other unknown mechanisms. Acquired lipodystrophies do not have a direct genetic basis. Some researchers have speculated that individuals may have a genetic predisposition to developing certain forms of acquired lipodystrophy, however, this remains unproven and controversial. Most likely, several different underlying mechanisms are involved in the development of acquired lipodystrophies.
AGL may occur following an infection or autoimmune disease. Infections that have preceded the onset of AGL include varicella, measles, pertussis, diphtheria, pneumonia, osteomyelitis, infectious mononucleosis and parotitis. Autoimmune disorders that have been linked to AGL include autoimmune thyroiditis, autoimmune hepatitis, juvenile dermatomyositis, rheumatoid arthritis, Sjogren’s syndrome, Sicca syndrome and autoimmune hemolytic anemia. Some people have low levels in their blood of complement 4, a protein factor that normally plays a role in the body’s immune system response. Recently, PLIN1 autoantibodies have been identified in the blood of a subset of patients with AGL which may be associated with destruction of fat cells. In many people, the cause of AGL is unknown.
APL is thought to be caused because the immune system mistakenly brings about the destruction of fat cells (autoimmune-mediated destruction of adipocytes). About 70% of affected individuals have low levels in their blood of complement 3, a protein factor that normally plays a role in the body’s immune system response. Affected individuals also have a circulating autoantibody called complement 3-nephritic factor. However, the precise autoantibody associated with destruction of fat cells in people with APL has not been identified.
Both AGL and APL may be associated with abnormal levels complement proteins in blood, which are specialized proteins that help fight off infection and disease. These proteins are also thought to be involved in the metabolic functions associated with body fat (adipose tissue). These proteins may render fat cells susceptible to improper destruction by the immune system.
The exact reason why therapy with protease inhibitors and reverse transcriptase inhibitors (nucleoside analogues) in individuals with HIV causes lipodystrophy is not fully understood.
Localized lipodystrophy may be caused by the injection of various drugs, such as insulin, into the subcutaneous tissue. Panniculitis, pressure on a specific area of the body, and other mechanisms may also cause localized lipodystrophy.
The underlying issue in individuals with acquired lipodystrophy is the complete or partial loss of adipose tissue. The primary role of adipose tissue is to store fat for energy. Adipose tissue also secretes a variety of molecules that are involved with or influence various hormonal functions. For example, patients with AGL may have reduced levels of leptin, a hormone or cytokine produced by adipose cells which plays a role in controlling appetite by working centrally in the brain and hypothalamus. Adipose tissue is made up of fat cells (adipocytes). Each adipocyte has a lipid droplet that accounts for approximately 90% of its cell volume. An adipocyte stores fats (triglycerides) within its lipid droplet.
The protein Perilipin 1 (PLIN1) produced by the PLIN1 gene, located on the surface of lipid droplets, is crucial for lipid droplet (LD) regulation in fat cells, and its dysfunction links to metabolic diseases like obesity, severe lipodystrophies, and insulin resistance/type 2 diabetes, often through altered lipolysis. PLIN1 gene variants cause familial partial lipodystrophy with diabetes, while anti-PLIN1 antibodies are biomarkers for acquired lipodystrophy (AGL).
Damage to adipose tissue in acquired lipodystrophy prevents proper fat storage. Consequently, fat is lost from adipose tissue, and in some people is improperly stored in other tissue of the body such as the liver and skeletal muscle causing symptoms such as liver disease and insulin resistance.
AGL and APL generally affect females more than males, although this may be due in part to ascertainment bias because females tend to be more severely affected and more easily recognized. APL has been reported in approximately 250 individuals with a male to female ratio of 1:4. It has been reported in individuals of various ethnicities. AGL has been reported in approximately 100 individuals with a male to female ratio of 1:3. Most cases have been reported in Caucasians. LD-HIV is estimated to affect approximately 100,000 individuals in the United States. Consistent with the increase prevalence of HIV in males, LD-HIV is also more prevalent in males.
A diagnosis of an acquired lipodystrophies is based upon identification of characteristic symptoms, a detailed patient history, a thorough clinical evaluation and a variety of specialized tests. AGL may be suspected in people who have a generalized lack of subcutaneous fat and overall muscular appearance during childhood.
The presence of panniculitis preceding the development of lipodystrophy is supportive of a diagnosis of AGL. The presence of an autoimmune disease preceding the development of lipodystrophy is supportive of AGL or APL. With APL, a progressive loss of fat from the upper body that spares the lower body in children under the age of 16 is suggestive of a diagnosis.
Clinical Testing and Workup
Although the diagnosis of lipodystrophy is primarily clinical, a variety of tests can be used to aid in the diagnosis and/or rule out other conditions. A blood chemical profile may be conducted to assess the levels of glucose, lipids, liver enzymes and uric acid. People with APL may have decreased serum C3 levels, normal C1 and C4 levels and high levels of the autoantibody C3NeF, while some people with AGL may have low serum C4 levels. PLIN1 autoantibody testing will likely be available soon in clinical laboratories for patients with AGL. At present, it is available only in research laboratories.
The characteristic pattern of fat loss in acquired lipodystrophies can be noted on whole body magnetic resonance imaging (MRI).
A renal biopsy, the surgical removal and microscopic examination of kidney tissue, may be performed to assess kidney involvement in individuals with APL.
Treatment
The treatment of acquired lipodystrophies is directed toward the specific symptoms that are apparent in each individual. Treatment may require the coordinated efforts of a team of specialists. Pediatricians, plastic surgeons, cardiologists, endocrinologists, nutritionists and other healthcare professionals may need to systematically and comprehensively plan an affected child’s treatment.
Individuals with acquired lipodystrophies and their families are encouraged to seek counseling after a diagnosis because the diagnosis can cause anxiety, stress and extreme psychological distress. Psychological support and counseling both professionally and through support groups is recommended for affected individuals and their families. Genetic counseling may be helpful for patients and their families as well.
Despite the lack of clinical trial evaluation, individuals with acquired lipodystrophy and severe hypertriglyceridemia are encouraged to follow a very-low-fat diet (<10–15% of calories or <20–40 g fat/day) to reduce chylomicronemia and lower the risk of acute pancreatitis. Such a diet can improve chylomicronemia associated with acute pancreatitis. Chylomicronemia is a condition characterized by the accumulation of fatty droplets called chylomicrons in the plasma. However, such diets may also raise very low-density lipoprotein triglyceride concentration. Nutrition therapy should be individualized with a registered dietitian familiar with lipodystrophy.
Regular exercise and maintaining a healthy weight are also encouraged to decrease the chances of developing diabetes. In individuals with acquired lipodystrophy, exercise and reducing energy intake is also necessary to avoid excess fat deposition and accumulation in non-lipodystrophic areas such as the face or neck.
Individuals with extreme hypertriglyceridemia may be treated with fibric acid derivatives, statins, or n-3 polyunsaturated fatty acids supplementation from fish oils.
The characteristic loss of adipose tissue in individuals with acquired lipodystrophy cannot be reversed. Consequently, cosmetic surgery may be beneficial in improving appearance. Procedures such as liposuction can be performed to remove excess unwanted fat in areas where fat accumulates (e.g. chin).
In some people, liver disease associated with acquired lipodystrophy can ultimately require a liver transplantation.
Additional therapies to treat individuals with acquired lipodystrophy are symptomatic and supportive and follow regular, standard guidelines. Diabetes is treated with standard therapies. After the onset of diabetes, hyperglycemic drugs such as metformin, sulfonylureas, thiazolidinediones and other agents may be recommended to treat hyperglycemia, although their long-term safety and efficacy is unknown. Insulin can also be used to treat individuals with acquired lipodystrophy and diabetes, although extremely high doses are often required. Medications to treat high blood pressure (anti-hypertensives) may also be recommended. Although drug therapy is commonly used, there have been no clinical trials to establish the optimal use of drug therapy to treat the metabolic complications in individuals with acquired lipodystrophy.
In 2014, metreleptin (an analogue of leptin) was approved by the U.S. Food and Drug Administration (FDA) for patients with generalized lipodystrophies including AGL and congenital generalized lipodystrophy. An analog drug has the same or similar physical structure to another drug or chemical but differs chemically. Severe lipodystrophy is sometimes associated with leptin deficiency. Studies showed that leptin-replacement therapy (metreleptin) improved the symptoms of AGL including hyperglycemia and hypertriglyceridemia and reduced liver size. However, drug related risks, cost and benefits should be carefully weighed prior to considering the treatment. Metreleptin therapy has been associated with two important side effects (black box warnings): development of neutralizing anti-leptin antibodies and lymphomas in patients with AGL.
While the exact health effects of neutralizing anti-leptin antibodies are not fully understood, these antibodies may reduce the effectiveness of metreleptin and interfere with normal leptin activity. The relationship between metreleptin therapy and the development of lymphoma is not clearly established, as lymphomas have also been reported in patients with acquired generalized lipodystrophy who were never treated with metreleptin. Metreleptin is not approved for the treatment of metabolic complications in patients with partial or localized forms of lipodystrophy, including acquired partial lipodystrophy or HIV-associated lipodystrophy.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at UT Southwestern Medical Center at Dallas, visit the webpage, https://utswmed.org/doctors/abhimanyu-garg/lipodystrophy-and-adipose-tissue-disorders/.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Toll-free: (800) 411-1222
TTY: (866) 411-1010
Email: [email protected]
For information about clinical trials sponsored by private sources, in the main, contact:
www.centerwatch.com
For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/
Contact for additional information about acquired lipodystrophy:
Abhimanyu Garg, MD
Professor of Internal Medicine
Chief, Section of Nutrition and Metabolic Diseases
Division of Endocrinology
Distinguished Chair in Human Nutrition Research
Center for Human Nutrition
UT Southwestern Medical Center
5323 Harry Hines Boulevard, K5.214
Dallas, TX 75390-8537
Phone: 214-648-2895
Fax: 214-648-0553
TEXTBOOKS
Garg A. Lipodystrophies and dyslipidemia. In Garg A (ed). Dyslipidemias: Pathophysiology, Evaluation and Management. Springer, New York, NY. 2015:287-302.
Simha V, Agarwal A. Inherited and Acquired Lipodystrophies. In: Nutrition and Health: Adipose Tissue and Adipokines in Health and Disease, Fantuzzi G, Mazzone T, editors. Humana Press, Totowa, NJ. 2007:237-254.
Garg A. Acquired Generalized Lipodystrophy. NORD Guide to Rare Disorders. Lippincott Williams & Wilkins. Philadelphia, PA. 2003:320.
Garg A. Acquired Partial Lipodystrophy. NORD Guide to Rare Disorders. Lippincott Williams & Wilkins. Philadelphia, PA. 2003:321.
JOURNAL ARTICLES
Kaewkrasaesin C, Hwang M, Vasandani C, Brown RJ, Garg A. Clinical features, metabolic and autoimmune derangements in acquired partial lipodystrophy (Barraquer-Simons Syndrome). J Clin Endocrinol Metab. Published online May 28, 2025. doi:10.1210/clinem/dgaf315
Mandel-Brehm C, Vazquez SE, Liverman C, et al. Autoantibodies to Perilipin-1 Define a Subset of Acquired Generalized Lipodystrophy. Diabetes. 2023;72(1):59-70. doi:10.2337/db21-1172
Diker-Cohen T, Cochran E, Gorden P, Brown RJ. Partial and generalized lipodystrophy: comparison of baseline characteristics and response to metreleptin. J Clin Endocrinol Metab. 2015;100(5):1802-1810. doi:10.1210/jc.2014-4491
Garg A. Clinical review: lipodystrophies: genetic and acquired body fat disorders. J Clin Endocrinol Metab. 2011;96:3313-3325. https://www.ncbi.nlm.nih.gov/pubmed/21865368
Savage DB, Semple RK, Clatworthy MR, et al. Complement abnormalities in acquired lipodystrophy revisited. J Clin Endocrinol Metab. 2009;94:10-16. https://www.ncbi.nlm.nih.gov/pubmed/18854390
Bingham A, Mamyrova G, Rother KI, et al. Predictors of acquired lipodystrophy in juvenile-onset dermatomyositis and a gradient of severity. Medicine (Baltimore). 2008;87:70-86. https://www.ncbi.nlm.nih.gov/pubmed/18344805
Hegele RA, Joy TR, Al-Attar SA, Rutt BK. Thematic review series: adipocyte biology. Lipodystrophies: windows on adipose biology and metabolism. J Lipid Res. 2007;48:1433-1444. https://www.ncbi.nlm.nih.gov/pubmed/17374881
Garg A. Acquired and inherited lipodystrophies. N Engl J Med. 2004;350:1220-1234. https://www.ncbi.nlm.nih.gov/pubmed/15028826
Misra A, Peethambaram A, Garg A. Clinical features and metabolic and autoimmune derangements in acquired partial lipodystrophy: report of 35 cases and review of the literature. Medicine (Baltimore). 2004;83(1):18-34. doi:10.1097/01.md.0000111061.69212.59
Misra A, Garg A. Clinical features and metabolic derangements in acquired generalized lipodystrophy: case reports and review of the literature. Medicine (Baltimore). 2003;82:129-146. https://www.ncbi.nlm.nih.gov/pubmed/12640189
Oral EA, Simha V, Ruiz E. Leptin-replacement therapy for lipodystrophy. N Engl J Med. 2002;346:570-578. https://www.ncbi.nlm.nih.gov/pubmed/11856796
Fukumoto D, Kubo Y, Saito M, Arase S. Centrifugal lipodystrophy of the scalp presenting with an arch-form alopecia: a 10-year follow-up observation. J Dermatol. 2009;36(9):499-503. doi:10.1111/j.1346-8138.2009.00685.x
Sharawat IK, Dawman L. Localized Lipodystrophy following Single Dose Intramuscular Gentamycin Injection. Indian Dermatol Online J. 2017;8(5):373-374. doi:10.4103/idoj.IDOJ_390_16
Serrão VV, Feio AB. Localized abdominal idiopathic lipodystrophy. Dermatol Online J. 2008;14(7):15. Published 2008 Jul 15.
Levy J, Burnett ME, Magro CM. Lipophagic Panniculitis of Childhood: A Case Report and Comprehensive Review of the Literature. Am J Dermatopathol. 2017;39(3):217-224. doi:10.1097/DAD.0000000000000721
Presta F, Del Giglio M, Girolomoni G. Lipoatrophia semicircularis: a case report and review of the literature. G Ital Dermatol Venereol. 2016;151(4):441-444.
INTERNET
Oral EA. Generalized Lipodystrophy. Medscape. Dec 12, 2022. https://emedicine.medscape.com/article/128355-overview Accessed June 2, 2025.
Partial Acquired Lipodystrophy. Orphanet. October 2019. Available at: https://www.orpha.net/en/disease/detail/79087?name=Partial%20Acquired%20Lipodystrophy&mode=name Accessed June 2, 2025.
Congenital generalized lipodystrophy. Orphanet. December 2020. Available at: https://www.orpha.net/en/disease/detail/528?name=Congenital%20lipodystrophy&mode=name Accessed June 2, 2025.
Lipodystrophy and Adipose Tissue Disorders. UTSouthwestern Medical Center. Available at https://utswmed.org/doctors/abhimanyu-garg/lipodystrophy-and-adipose-tissue-disorders/?_ga=2.140515444.773001568.1748427276-1089408249.1748427276 Accessed June 2, 2025.
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