Zinc-α2-glycoprotein promotes browning of white adipose tissue in cold-exposed male mice

Fan, Guoqiang; Dang, Xiaobo; Li, Yanfei; Chen, Jinglong; Zhao, Ruqian; Yang, Xia

doi:10.1016/j.mce.2019.110669

Cited by 14 publications

(8 citation statements)

References 36 publications

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“…ZAG is mainly synthesized in the adipose tissue and secreted into the blood to enter other tissues or organs where it fulfills its functions. Our previous study showed that cold stress leads to a markedly higher plasma content of ZAG in WT mice compare to the ZAG KO mice [17]. In the present study, knocking-out ZAG significantly influenced TG content in the gastrocnemius mus-cle after the cold stress treatment.…”

Section: Endocrine Journal Advance Publicationsupporting

confidence: 53%

“…Previous studies have shown that cold stress promotes browning of adipocytes, and enhances the occurrence of the heat generation process [27]. In our previous study, thermogenesis by the brown and white adipose tissues had significantly increased in WT mice compared to ZAG KO mice who experienced cold stress [17]. Brown adipose tissue and skeletal muscle are two well-known sites of thermogenesis [3,28,29].…”

Section: Endocrine Journal Advance Publicationmentioning

confidence: 76%

“…ZAG protein is mainly synthesized in the adipose tissue, and the expression of ZAG in skeletal muscle is relatively less compared to adipose tissue. Our previous study showed that the ZAG protein expression was significantly increased after injection of ZAG plasmids in adipose tissue [17]. ZAG in adipose tissue is secreted into the blood, where it travels to skeletal muscles and acts.…”

Section: Endocrine Journal Advance Publicationmentioning

confidence: 99%

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Zinc-α2-glycoprotein promotes skeletal muscle lipid metabolism in cold-stressed mice

Fan

et al. 2021

Endocr J

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Skeletal muscle is the most abundant tissue in the adult body and plays an essential role in maintaining heat production for the entire body. Recently, muscle-derived non-shivering thermogenesis under cold conditions has received much attention. Zinc-α2-glycoprotein (ZAG) is an adipokine that was shown to influence energy metabolism in the adipose tissue. We used ZAG knock-out (ZAG KO) and wild-type (WT) mice to investigate the effect of ZAG on the lipid metabolism of skeletal muscle upon exposure to a low temperature (6°C) for one week. The results show that cold stress significantly increases the level of lipolysis, energy metabolism, and fat browning-related proteins in the gastrocnemius muscle of WT mice. In contrast, ZAG KO mice did not show any corresponding changes. Increased expression of β3-adrenoceptor (β3-AR) and protein kinase A (PKA) might be involved in the ZAG pathway in mice exposed cold stress. Furthermore, expression of lipolysis-related proteins (ATGL and p-HSL) and energy metabolism-related protein (PGC1α, UCP2, UCP3 and COX1) was significantly enhanced in ZAG KO mice after injection of ZAG-recombinant plasmids. These results indicate that ZAG promotes lipid-related metabolism in the skeletal muscle when the animals are exposed to low temperatures. This finding provides a promising target for the development of new therapeutic approaches to improve skeletal muscle energy metabolism.

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Section: Endocrine Journal Advance Publicationsupporting

confidence: 53%

Section: Endocrine Journal Advance Publicationmentioning

confidence: 76%

Section: Endocrine Journal Advance Publicationmentioning

confidence: 99%

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Zinc-α2-glycoprotein promotes skeletal muscle lipid metabolism in cold-stressed mice

Fan

et al. 2021

Endocr J

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“…Half of the samples from the OB2 and OB3 groups were also characterized by this diagnosis. As part of a pattern of 15 proteins for 5 (P07225 [ 35 ], O43866 [ 36 , 37 ], P02654 [ 38 ], P25311 [ 39 , 40 , 41 ], P29622 [ 42 ]) the association with the obesity was shown. It is noteworthy that five of these 15 proteins are complement components, included in two complexes: P07358, P07357, and P13671 organize membrane attack complex (MAC), that plays a key role in the innate and adaptive immune response, and P09871 and P00736 combine with serine protease to form the first component of the classical and less variable pathway of the complement system, also associated with obesity [ 43 , 44 ].…”

Section: Resultsmentioning

confidence: 99%

Does Proteomic Mirror Reflect Clinical Characteristics of Obesity?

Kiseleva

Arzumanian

Poverennaya

et al. 2021

JPM

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Obesity is a frightening chronic disease, which has tripled since 1975. It is not expected to slow down staying one of the leading cases of preventable death and resulting in an increased clinical and economic burden. Poor lifestyle choices and excessive intake of “cheap calories” are major contributors to obesity, triggering type 2 diabetes, cardiovascular diseases, and other comorbidities. Understanding the molecular mechanisms responsible for development of obesity is essential as it might result in the introducing of anti-obesity targets and early-stage obesity biomarkers, allowing the distinction between metabolic syndromes. The complex nature of this disease, coupled with the phenomenon of metabolically healthy obesity, inspired us to perform data-centric, hypothesis-generating pilot research, aimed to find correlations between parameters of classic clinical blood tests and proteomic profiles of 104 lean and obese subjects. As the result, we assembled patterns of proteins, which presence or absence allows predicting the weight of the patient fairly well. We believe that such proteomic patterns with high prediction power should facilitate the translation of potential candidates into biomarkers of clinical use for early-stage stratification of obesity therapy.

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“…A potential link been ZAG and the metabolic activity of visceral adipose tissue is important given the deleterious impact of visceral fat to metabolic health (46) and the risk of T2DM. In the opposite direction, higher levels and greater expression of ZAG have been associated with the browning of adipose tissue, which could have positive implications to metabolic health (47).…”

Section: Discussionmentioning

confidence: 99%

Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis

Pearsey

Henson

Sargeant

et al. 2020

Rev Endocr Metab Disord

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To systematically review the current literature investigating associations between zinc-alpha2-glycoprotein (ZAG) and dysglycaemia (including type 2 diabetes (T2DM), poly-cystic-ovary syndrome (PCOS), pre-diabetes or insulin resistance). This included relationships between ZAG and continuous measures of insulin and glucose. Additionally, we performed a meta-analysis to estimate the extent that ZAG differs between individuals with or without dysglycaemia; whilst examining the potential influence of adiposity. A systematic search was performed on four databases for studies on circulating ZAG concentrations in adult human populations, comparing healthy controls to individuals with dysglycaemia. Key characteristics, including the mean ZAG concentrations (mg∙L−1), and any correlational statistics between ZAG and continuous measures of glucose, glycated haemoglobin (HbA1c) or insulin were extracted. Meta-analyses were performed to compare metabolically healthy controls to cases, and on studies that compared controls and cases considered overweight or obese (body mass index (BMI) ≥25 kg.m2). 1575 papers were identified and 14 studies (16 cohorts) were considered eligible for inclusion. Circulating ZAG was lower in individuals with dysglycaemia compared to metabolically healthy controls (−4.14 [−8.17, −0.11] mg.L−1; I2 = 98.5%; p < 0.001). When using data from only studies with overweight or obese groups with or without dysglycaemia (three studies (four cohorts); pooled n = 332), the difference in circulating ZAG was no longer significant (−0.30 [−3.67, 3.07] mg. L−1; I2 = 28.0%; p = 0.225). These data suggest that ZAG may be implicated in dysglycaemia, although there was significant heterogeneity across different studies and the mediating effect of adiposity cannot be excluded. Therefore, more research is needed before robust conclusions can be drawn.

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Zinc-α2-glycoprotein promotes browning of white adipose tissue in cold-exposed male mice

Cited by 14 publications

References 36 publications

Zinc-α2-glycoprotein promotes skeletal muscle lipid metabolism in cold-stressed mice

Zinc-α2-glycoprotein promotes skeletal muscle lipid metabolism in cold-stressed mice

Does Proteomic Mirror Reflect Clinical Characteristics of Obesity?

Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis

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