Circulating serum chemerin levels are elevated in lipodystrophy

Miehle, Konstanze; Ebert, Thomas; Kralisch, Susan; Hoffmann, Annett; Kratzsch, Jürgen; Schlögl, Haiko; Stümvoll, Michael; Faßhauer, Mathias

doi:10.1111/cen.12976

Cited by 8 publications

(3 citation statements)

References 35 publications

(107 reference statements)

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“…In this regard, previous studies report conflicting results on chemerin levels in different diseases with an inflammatory component such as chronic pancreatitis (94.0 ng/mL) [ 40 ], T2DM individuals (179.0 ng/mL) [ 41 ], lipodystrophy (234.3 ng/mL) [ 42 ], and obesity without diabetes (590.08 ng/mL) [ 43 ]. Chemerin levels were increased, except for the levels reported in rheumatoid arthritis (35.0 ng/mL) [ 44 ] (an inflammatory disease per se ), although this can be explained based on treatment; however, other studies have suggested that chemerin may be the functional link between chronic inflammation and obesity-related T2DM and cardiovascular disease [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Inverse Relationship of theCMKLR1Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance

Corona-Meraz

Navarro-Hernández

Ruiz-Quezada

et al. 2016

Mediators of Inflammation

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Background. In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressed CMKLR1 receptor. The role of chemerin and CMKLR1 in inflammatory process secondary to obesity is not defined yet. Methods. Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression of CMKLR1 were evaluated with qPCR and 2−ΔΔCT method. Results. Differences (P < 0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. Both CMKLR1 expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r = 8.8% to 38.5%), P < 0.05. Conclusion. The increment of CMKLR1 expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin and CMKLR1 have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.

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Section: Discussionmentioning

confidence: 99%

Inverse Relationship of theCMKLR1Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance

Corona-Meraz

Navarro-Hernández

Ruiz-Quezada

et al. 2016

Mediators of Inflammation

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“…Metreleptin doses from second week onwards ranged from 2.5 to 7.8 mg per day. [ 54 ]. Lipid-lowering and antihyperglycemic medication was modified if necessary.…”

Section: Methodsmentioning

confidence: 99%

Increased Growth Differentiation Factor 15 in Patients with Hypoleptinemia-Associated Lipodystrophy

Kralisch

Hoffmann

Estrada-Kunz

et al. 2020

IJMS

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Objective. Similar to obesity, lipodystrophy (LD) causes adipose tissue dysfunction and severe metabolic complications. Growth differentiation factor 15 (GDF15) belongs to the transforming growth factor β superfamily and is dysregulated in metabolic disease including obesity and diabetes mellitus. Circulating levels in LD and the impact of leptin treatment have not been investigated so far. Material and Methods. GDF15 serum levels were quantified in 60 LD patients without human immunodeficiency virus infection and 60 controls matched for age, gender, and body mass index. The impact of metreleptin treatment on circulating GDF15 was assessed in a subgroup of patients. GDF15 mRNA expression was determined in metabolic tissues of leptin-deficient lipodystrophic aP2-nSREBP1c-Tg mice, obese ob/ob mice, and control C57Bl6 mice. Results. Median GDF15 serum concentrations were significantly higher in LD patients (819 ng/L) as compared to the control group (415 ng/L) (p < 0.001). In multiple linear regression analysis, an independent and positive association remained between GDF15 on one hand and age, patient group, hemoglobin A1c, triglycerides, and C-reactive protein on the other hand. Moreover, there was an independent negative association between GFD15 and estimated glomerular filtration rate. Circulating GDF15 was not significantly affected by metreleptin treatment in LD patients. Gdf15 was upregulated in leptin-deficient lipodystrophic mice as compared to controls. Moreover, Gdf15 mRNA expression was downregulated by leptin treatment in lipodystrophic and obese animals. Conclusions. Serum concentrations of GDF15 are elevated in LD patients and independently associated with markers of metabolic dysfunction. Gdf15 expression is higher in lipodystrophic mice and downregulated by leptin treatment.

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“…Patients with LD suffer from a number of metabolic disorders similar to morbid obesity such as severe insulin resistance, hyperlipidemia, and hepatic steatosis due to the ectopic accumulation of fat in skeletal muscle, pancreas, and liver [ 1 ]. In addition, because of the lack of adipose tissue, several metabolically important adipokines are dysregulated in patients with LD, including leptin [ 2 ], adiponectin [ 2 ], and progranulin [ 3 ], amongst others [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Leptin Improves Parameters of Brown Adipose Tissue Thermogenesis in Lipodystrophic Mice

et al. 2021

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Lipodystrophy syndromes (LD) are a heterogeneous group of very rare congenital or acquired disorders characterized by a generalized or partial lack of adipose tissue. They are strongly associated with severe metabolic dysfunction due to ectopic fat accumulation in the liver and other organs and the dysregulation of several key adipokines, including leptin. Treatment with leptin or its analogues is therefore sufficient to reverse some of the metabolic symptoms of LD in patients and in mouse models through distinct mechanisms. Brown adipose tissue (BAT) thermogenesis has emerged as an important regulator of systemic metabolism in rodents and in humans, but it is poorly understood how leptin impacts BAT in LD. Here, we show in transgenic C57Bl/6 mice overexpressing sterol regulatory element-binding protein 1c in adipose tissue (Tg (aP2-nSREBP1c)), an established model of congenital LD, that daily subcutaneous administration of 3 mg/kg leptin for 6 to 8 weeks increases body temperature without affecting food intake or body weight. This is associated with increased protein expression of the thermogenic molecule uncoupling protein 1 (UCP1) and the sympathetic nerve marker tyrosine hydroxylase (TH) in BAT. These findings suggest that leptin treatment in LD stimulates BAT thermogenesis through sympathetic nerves, which might contribute to some of its metabolic benefits by providing a healthy reservoir for excess circulating nutrients.

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Circulating serum chemerin levels are elevated in lipodystrophy

Abstract: Circulating levels of the adipokine chemerin are elevated in LD, as well as independently and positively associated with HbA1c and CRP. Increased chemerin might originate from VAT and BAT.

Cited by 8 publications

References 35 publications

Inverse Relationship of theCMKLR1Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance

Inverse Relationship of theCMKLR1Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance

Increased Growth Differentiation Factor 15 in Patients with Hypoleptinemia-Associated Lipodystrophy

Leptin Improves Parameters of Brown Adipose Tissue Thermogenesis in Lipodystrophic Mice

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