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Adipose tissue biology and effect of weight loss in women with lipedema

ABSTRACT: Lipedema is a lipodystrophic disease characterized by marked increases in lower-body subcutaneous adipose tissue, anecdotally reported to: i) increase inflammation and fibrosis and impair microvascular and lymphatic circulation in the affected adipose tissue, ii) reduce risk of developing obesity-related cardiometabolic abnormalities; and iii) be resistant to diet-induced weight loss. To further our understanding of lipedema, we examined body composition, metabolic health and adipose tissue bology in women with obesity and lipedema (Obese-LIP) at baseline and following ~9% diet-induced weight loss. At baseline, people with Obese-LIP had ~23% greater leg fat mass, ~11% lower android-to-gynoid ratio and ~54% greater insulin sensitivity compared to women matched on age, body mass index and whole-body fat mass. In the Obese-LIP group, total and proinflammatory macrophage content and expression of inflammation and fibrosis-related genes were greater while lymph/angiogenesis-related genes were lower in subcutaneous femoral compared to abdominal adipose tissue. Diet-induced weight loss improved insulin sensitivity and decreased total fat mass due to similar reductions in abdominal and leg fat masses, with minimal effect on markers of adipose tissue inflammation/fibrosis and lymph/angiogenesis. Our study provides important insights into the pathophysiology of lipedema and suggests diet-induced weight loss should be the cornerstone therapy in people with Obese-LIP.

ORGANISM(S): Homo sapiens

PROVIDER: GSE274137 | GEO | 2024/10/15

REPOSITORIES: GEO

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Project description:Maternal obesity is linked with increased adverse outcomes for mother and fetus. However, the metabolic impact of excessive fat accumulation within the altered hormonal context of pregnancy is not well understood. We used a murine model of obesity, the high fat diet-fed C57BL/6J mouse to determine adipose tissue-mediated molecular mechanisms driving metabolic dysfunction throughout pregnancy. Remarkably, obese mice exhibited a normalization of visceral fat accumulation at late-stage pregnancy (-53%, P<0.001 E18.5) to achieve levels comparable in mass (per gram of body weight) to that of non pregnant, control diet fed mice. Moreover, whilst obese pregnant mice showed a marked glucose intolerance and apparent insulin resistance at mid-stage pregnancy (E14.5), glucose homeostasis converged with that of lean pregnant mice at late-stage pregnancy, suggesting an unexpected amelioration of the worsening metabolic dysfunction in obese pregnant mice. Transcriptomic analysis of the late-stage visceral fat indicated reduced de novo lipogenic drive (Me1, Fasn, Scd1, Dgat2), retinol metabolism (Rdh11, Rbp4) and inflammation (Mcp1, Tnfα) in obese pregnant mice that was confirmed functionally by their lower adipose proinflammatory macrophage density. Elevated expression of estrogen receptor a (ERα) in visceral adipose tissue was identified as potential unifying mechanism for the transcriptional changes and reduced adiposity of late stage obese pregnancy. Support for a role for ERα was provided by experiments showing that the ERα selective agonist PPT suppressed lipogenesis in primary mouse adipocytes and suppressed Me1, Fasn, SCD1 and Dgat2 mRNA levels in mature female human ChubS7 clonal fat cells. Our data reveal a novel role for elevated visceral adipocyte estrogen signaling as a protective mechanism against visceral fat hypertrophy and inflammation in late pregnancy. Pregnant high fat, pregnant control fat, non pregnant high fat, non pregnant control fat. Five biologial replictes each (20 samples).

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Adipose tissue biology and effect of weight loss in women with lipedema

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