Failure to Detect Brown Adipose Tissue Uncoupling Protein mRNA in Benign Symmetric Lipomatosis (Madelung's Disease).

Kazumi, Tsutomu; Ricquier, Daniel; Maeda, Toshihisa; Masuda, Tadayuki; Hozumi, Toshiki; Ishida, Yukinori; Yoshida, Midori

doi:10.1507/endocrj.41.315

Cited by 8 publications

(9 citation statements)

References 12 publications

(18 reference statements)

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“…The hematoxylin-eosin staining did not show any differences between the affected and unaffected fatty tissue. This agrees with the findings of some case reports, where macroscopically regular lobulated adipose tissue without any abnormalities was described in samples of affected fatty tissue from MSL patients [12][13][14]. Although Agostini et al [15] compared affected adipose tissue with unaffected adipose tissue in one patient with MSL and described dystrophic adipocytes with significantly enlarged fat vacuoles (30%) in the affected tissue, Pollock et al [16] described a diffuse spread of adipose tissue along nerve vein sheaths as well as in muscle compartments.…”

Section: Discussionsupporting

confidence: 93%

“…This suggests that not only the affected adipose tissue of MSL patients, but also the unaffected adipose tissue carries genetic alterations and would explain the progression of MSL in previously unaffected areas of the body. In contrast, Kazumi et al [12] were not able to detect any expression of UCP1 in the affected adipose tissue in an MSL patient. In a previous publication, we were already able to show an increase in UCP1 in real-time reversetranscriptase polymerase chain reaction analysis [12].…”

Section: Discussionmentioning

confidence: 74%

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Adipose Tissue in Multiple Symmetric Lipomatosis Shows Features of Brown/Beige Fat

et al. 2020

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Introduction Multiple symmetric lipomatosis (MSL) (syn.: Launois-Bensaude Syndrome, benign symmetric lipomatosis) is a rare disease of fatty tissue. The pathophysiology of MSL still remains unclear, although several approaches have been described in order to understand it. Beside morphological characteristics and some molecular cell biological approaches, little is known about the histological and immunohistochemical characterization of adipose tissue from patients with MSL. Methods From the 45 patients with MSL in our database, 10 were included in the study. Fat tissue samples were collected from affected and unaffected areas. The forearm served as a control area as this area is not affected in MSL. The specimens were analyzed after selected stainings were taken (hematoxylin-eosin = HE, Elastica van Gieson,

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 74%

Adipose Tissue in Multiple Symmetric Lipomatosis Shows Features of Brown/Beige Fat

et al. 2020

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“…However, it is important to emphasize the fact that unlike the control white subcutaneous adipocytes, the cells did express the UCP‐1 marker of brown adipocytes. Kazumi et al 32 failed to detect any UCP‐1 mRNA in MSL lipomas, but this may have been because they used northern blots; our RT‐PCR analysis is a more sensitive detector of poorly expressed UCP‐1 mRNA, as has also been shown by Vila et al 33 in one MSL patient.…”

Section: Discussionmentioning

confidence: 68%

Multiple symmetric lipomatosis may be the consequence of defective noradrenergic modulation of proliferation and differentiation of brown fat cells

Nisoli

Regianini

Briscini

et al. 2002

The Journal of Pathology

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Multiple symmetric lipomatosis (MSL) is an inherited disorder in which enlarging and unencapsulated lipomas symmetrically develop in the subcutaneous tissue of the neck, shoulders, mammary, and truncal regions. In some cases, it is associated with mitochondrial DNA abnormalities. The pathogenesis of MSL is completely unknown, although the fat deposits may be due to a neoplastic-like proliferation of functionally defective brown adipocytes. It has recently been demonstrated that the beta(3)-adrenergic receptor is the functionally relevant adrenergic receptor subtype in brown adipocytes and that its stimulation by noradrenaline (NA) modulates the expression of genes, such as uncoupling protein (UCP)-1 and inducible nitric oxide synthase (iNOS), involved in fat cell proliferation and differentiation. Furthermore, Trp64Arg mutation of the beta(3)-adrenoceptor has been implicated in lower NA activity in adipose tissues. The aim of this study was to investigate the molecular and functional characteristics of MSL adipocytes and to analyse the effects of nitric oxide (NO) on the proliferation/differentiation of MSL adipocytes in culture, and the relevance of putative noradrenergic deficit in the development of lipomas in MSL patients. Cultured MSL adipocytes were able to synthesize UCP-1 (the selective marker of brown adipocytes), but unlike that of normally functioning brown fat cells, the expression of the UCP-1 gene was not significantly induced by NA. NA is also defective in inducing iNOS gene expression, thus leading to reduced NO production and a consequent reduction in the anti-proliferative, adipogenic (mitochondrial biogenesis) effects of NA on MSL cells. Furthermore, the transcriptional peroxisome proliferator-activated receptor gamma co-activator-1 (PGC-1), which plays a key role in the sympathetic-stimulated mitochondrial biogenesis of brown adipocytes, is expressed but not induced by NA in MSL cells, as it is in brown adipocytes. The study did not find any association between beta(3)-adrenoceptor gene polymorphism and noradrenergic signalling defects in MSL subjects with or without mitochondrial DNA mutations.

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“…SAT cells from subjects with MSL express UCP-1 suggesting its origin as BAT [61,70] , but this is not substantiated in all cases [71] . Adrenergic receptors (AR) that respond to sympathetic input, such as the three subtypes of β-AR, β 1 -, β 2 -and β 3 -, promote lipolysis and energy expenditure.…”

Section: Physiology Of Msl Satmentioning

confidence: 87%

Rare adipose disorders (RADs) masquerading as obesity

2012

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Rare adipose disorders (RADs) including multiple symmetric lipomatosis (MSL), lipedema and Dercum's disease (DD) may be misdiagnosed as obesity. Lifestyle changes, such as reduced caloric intake and increased physical activity are standard care for obesity. Although lifestyle changes and bariatric surgery work effectively for the obesity component of RADs, these treatments do not routinely reduce the abnormal subcutaneous adipose tissue (SAT) of RADs. RAD SAT likely results from the growth of a brown stem cell population with secondary lymphatic dysfunction in MSL, or by primary vascular and lymphatic dysfunction in lipedema and DD. People with RADs do not lose SAT from caloric limitation and increased energy expenditure alone. In order to improve recognition of RADs apart from obesity, the diagnostic criteria, histology and pathophysiology of RADs are presented and contrasted to familial partial lipodystrophies, acquired partial lipodystrophies and obesity with which they may be confused. Treatment recommendations focus on evidencebased data and include lymphatic decongestive therapy, medications and supplements that support loss of RAD SAT. Associated RAD conditions including depression, anxiety and pain will improve as healthcare providers learn to identify and adopt alternative treatment regimens for the abnormal SAT component of RADs. Effective dietary and exercise regimens are needed in RAD populations to improve quality of life and construct advanced treatment regimens for future generations.

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Failure to Detect Brown Adipose Tissue Uncoupling Protein mRNA in Benign Symmetric Lipomatosis (Madelung's Disease).

Cited by 8 publications

References 12 publications

Adipose Tissue in Multiple Symmetric Lipomatosis Shows Features of Brown/Beige Fat

Adipose Tissue in Multiple Symmetric Lipomatosis Shows Features of Brown/Beige Fat

Multiple symmetric lipomatosis may be the consequence of defective noradrenergic modulation of proliferation and differentiation of brown fat cells

Rare adipose disorders (RADs) masquerading as obesity

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