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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and epidemiologic evidence has shown acanthosis nigricans to be closely related to defective tissue utilization of insulin in a number of previously recognized (e.g., obesity, lipodystrophy, and leprechaunism) as well as recently characterized (e.g., type A and type B syndromes) disorders. This article reviews the relationship of acanthosis nigricans to these insulin-resistant states. It also focuses attention on the possibility that interaction between excessive amounts of circulating insulin with insulin-like growth factor receptors on keratinocytes and dermal fibroblasts leads to the development of acanthosis nigricans.
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PMID:Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for acanthosis nigricans. 131 28

Mandibuloacral dysplasia (MAD) is a syndrome with onset in midchildhood. The predominant characteristics of MAD include flexion contractures; mandibular hypoplasia; loss of body fat; atrophic, speckled skin; and progressive osteolysis of the clavicles. We studied three males with MAD. Each had lipodystrophy of the extremities, with sparing of the face and neck. All had moderate hyperlipidemia. In response to oral glucose, each had a diabetic response, with peak insulin levels between 2870 and 22,960 pmol/L. Insulin-stimulated glucose disposal was determined in two patients with MAD. At an insulin infusion rate of 120 mU/m2 per minute, glucose disposal was less than 25% of that measured at similar levels of insulinemia in nondiabetic control subjects, indicating marked insulin resistance in patients with MAD. The insulin resistance occurred without obesity, excessive levels of counterregulatory hormones, or anti-insulin-receptor antibodies. We suggest that MAD is a previously undescribed form of lipodystrophic insulin-resistant diabetes mellitus.
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PMID:Severe insulin resistance and diabetes mellitus in mandibuloacral dysplasia. 173 53

Forty-two patients with nonalcoholic steatohepatitis were followed for a median of 4.5 yr (range = 1.5 to 21.5 yr). Except for two patients with lipodystrophy, all were obese; 35 of 42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Initial liver biopsy specimens showed the presence of macrovesicular fatty infiltration, lobular (acinar) inflammation, apoptosis, Mallory bodies (in four cases) and fibrosis (in 18 cases). Cirrhosis was present at initial diagnosis in one subject and in another two subjects liver biopsy showed marked fibrosis with disturbed architecture. Serial liver biopsy specimens revealed minimal or no apparent progression of the disorder in most of the patients, in keeping with their benign clinical course. However, one patient showed progression from fibrosis to cirrhosis during the 5-yr observation period, and in the patients with extensive fibrosis the liver disease evolved from one of active inflammation to one of inactive cirrhosis without fat or inflammation. The patient with cirrhosis later died of hepatocellular carcinoma. The severity or type of hepatic change did not correlate with the degree of obesity, hyperlipidemia or hyperglycemia. However, in individual patients, poorly controlled diabetes and rapid weight loss preceded the onset of steatohepatitis. We conclude that nonalcoholic steatohepatitis is a cause of hepatic inflammation histologically resembling that of alcohol-induced liver disease but usually slowly progressive and of low-grade severity. However, the disorder may ultimately result in cirrhosis. Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of "cryptogenic cirrhosis."
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PMID:The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years. 1503 Sep 72

Two patients who presented with steatohepatitis had acquired partial lipodystrophy. This association has not previously been well documented. A common pathophysiological mechanism in lipodystrophy, obesity-associated nonalcoholic steatohepatitis, and alcoholic liver disease is possible.
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PMID:Steatohepatitis associated with limb lipodystrophy. 277 26

Lipodystrophy, almost exclusively seen in female patients, causes psychological problems at an early age. In later life, additional complaints are heavy painful legs, edema, and varicose veins. Nearly all patients suffer from alimentary adiposity. Dermolipectomies in general are not advisable because of the resulting large scars and the risk of damaging the lymphatic system. Subcutaneous lipectomy according to the Illouz method can provide good results. Weight loss is a good alternative to liposuction of the upper legs. After sufficient weight loss, only additional liposuction of the trochanteric area and the medial side of the knee is needed. No unpleasant scarring of the leg results. Unfortunately, older patients often require a skin reduction. The results of surgery in the lower legs were, except in 2 patients, good to excellent. The results in the upper legs were disappointing because 9 of 11 patients gained weight again after surgery. Considering this, the preferable treatment now is liposuction of the lower legs, medial side of the knee, and the trochanteric area. Only in cases of ptotic skin on the medial side of the upper legs is skin reduction without lipectomy indicated. Lipodystrophy suggests a disappearance of the subcutaneous fat. When this occurs in the upper part of the body, it is called progressive lipodystrophy. Lipodystrophy is known as an abnormality of the lower half of the female body, swollen by deposition of subcutaneous fat and determined by heredity. It occurs more frequently in the lower social classes and is often accompanied by an alimentary obesity which is a psychological reaction to the disturbed body image.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipodystrophy and its treatment. 323 31

The standard excisional approach to lipectomy has now been expanded by the use of suction curettage either as an adjunct or a primary procedure. In severe cases of steatomeria (a term used to designate trochanteric obesity and eliminate the misuse of the term lipodystrophy), curettage serves to prepare and shape the flaps, while excision and "periosteal dermal suspension" are sometimes necessary to achieve adequate contour and lift. Periosteal anchoring ensures adequate permanent suspension and a tension-free closure. Achievement of lateral thigh contouring by an anterior approach is facilitated by the use of the suction curette. Undermining of the superior flap and contouring with suction, as well as overlapping the closure with buried dermal-fat suspension flaps, eliminates bulging above or below the incision. Periosteal dermal suspension decreases the possibility of scar widening and eventual ptosis, provides a fixation technique that permits more lift, and eliminates scarring from the lateral thigh. Lateral thigh suction lipectomy with periosteal dermal suspension has been done alone or in conjunction with buttock reduction or with medial thigh or abdominal lipectomy in 14 patients. The operating time was short, and the results were good with minimal morbidity.
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PMID:Anterior periosteal dermal suspension with suction curettage for lateral thigh lipectomy. 676 69

A 79-year-old woman presented with an unusual form of obesity limited to the lower half of the body from the waistline down but sparing the lower legs and feet. The patient was massive (360 lbs) and symmetrical. The superior half of the body was normal with no morbid obesity or lipoatrophy. These findings do not correspond to any classic form of lipodystrophy. The fat distribution is reminiscent of a pair of knickers and qualifies for the name "pantaloon obesity."
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PMID:A case of pantaloon obesity. 686 15

Transgenic mice overexpressing a constitutively active human TGF-beta1 under control of the rat phosphoenolpyruvate carboxykinase regulatory sequences developed fibrosis of the liver, kidney, and adipose tissue, and exhibited a severe reduction in body fat. Expression of the transgene in hepatocytes resulted in increased collagen deposition, altered lobular organization, increased hepatocyte turnover, and in extreme cases, hemorrhage and thrombosis. Renal expression of the transgene was localized to the proximal tubule epithelium, and was associated with tubulointerstitial fibrosis, characterized by excessive collagen deposition and increased fibronectin and plasminogen activator inhibitor-1 immunoreactivity. Pronounced glomerulosclerosis was evident, and hydronephrosis developed with low penetrance. Expression of TGF-beta1 in white and brown adipose tissue resulted in a lipodystrophy-like syndrome. All white fat depots and brown fat pads were severely reduced in size, and exhibited prominent fibroplasia. This reduction in WAT was due to impaired adipose accretion. Introduction of the transgene into the ob/ob background suppressed the obesity characteristic of this mutation; however, transgenic mutant mice developed severe hepato- and splenomegaly. These studies strengthen the link between TGF-beta1 expression and fibrotic disease, and demonstrate the potency of TGF-beta1 in modulating mesenchymal cell differentiation in vivo.
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PMID:Hepatic fibrosis, glomerulosclerosis, and a lipodystrophy-like syndrome in PEPCK-TGF-beta1 transgenic mice. 938 33

The development of lipodystrophy as evidenced by central obesity, "moon facies," and a "buffalo hump" is a classical feature of Cushing's disease. Recently an association of "lipodystrophy" with the use of protease inhibitors has been reported. We describe a patient with lipodystrophy secondary to protease inhibitor therapy for HIV infection.
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PMID:Protease inhibitor-induced lipodystrophy. 1018 89

Recently, great progress has been made towards understanding the molecular basis of body fat regulation. Identification of mutations in several genes in spontaneous monogenic animal models of obesity and development of transgenic models have indicated the physiological roles of many genes in the regulation of body fat distribution. In humans, mutations in leptin, leptin receptor, prohormone convertase 1 (PC1), pro-opiomelanocortin (POMC), melanocortin 4-receptor (MC4-R), and peroxisome proliferator-activated receptor (PPAR) gamma2 genes have been described in patients with severe obesity. Most of these obesity disorders exhibit a distinct phenotype with varying degrees of hypothalamic and pituitary dysfunction and a recessive inheritance, whereas MC4-R mutation has a nonsyndromic phenotype with dominant inheritance. These mutations suggest the critical role of central signaling systems composed of leptin/leptin receptor and alpha-melanocyte stimulating hormone/MC4-R in human energy homeostasis. Although the genetic basis of monogenic disorders of body fat distribution, such as congenital generalized lipodystrophy and familial partial lipodystrophy, Dunnigan variety, is still unknown, the genes for these have recently been localized to chromosomes 9q34 and 1q21-22, respectively. The advances in our knowledge of the phenotypic manifestations and underlying molecular mechanisms of genetic body fat disorders may lead to better treatment and prevention of obesity and other disorders of adipose tissue in the future.
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PMID:Monogenic disorders of obesity and body fat distribution. 1050 93


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