Fat-Specific Knockout of Mecp2 Upregulates Slpi to Reduce Obesity by Enhancing Browning

Liu, Chengyu; Wang, Jiao; Wei, Yujuan; Zhang, Wenquan; Geng, Mengyuan; Yuan, Yangmian; Chen, Yu‐Chen; Sun, Yu; Chen, Hong; Zhang, Yu; Xiong, Mingrui; Li, Yangkai; Zheng, Ling; Huang, Kun

doi:10.2337/db19-0502

Cited by 30 publications

(34 citation statements)

References 48 publications

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“…Metabolic studies were performed as we previously described during the HF stage of the ninth cycle for HF‐LF cycled and matched HF mice using a Comprehensive Lab Animal Monitoring System (CLAMS, Columbus Instruments, Columbus, OH). O 2 consumption and activity were measured for each mouse over 3 days.…”

Section: Methodsmentioning

confidence: 99%

“…3T3‐L1 cells were cultured and differentiated as we previously reported . Mouse 3T3‐L1 cells were cultured in DMEM media (Hyclone, South Logan, UT) supplemented with 10% newborn bovine serum (Gibco) and 1% penicillin/streptomycin (Hyclone).…”

Section: Methodsmentioning

confidence: 99%

“…3T3-L1 cells were cultured and differentiated as we previously reported. 16,22 Mouse 3T3-L1 cells were cultured in DMEM media (Hyclone, South Logan, UT) supplemented with 10% newborn bovine serum (Gibco) and 1% penicillin/ streptomycin (Hyclone). Confluent 3T3-L1 cells (counted as Day -2) went through contact inhibition for 2 days and were induced in DMEM containing 10% FBS, 0.5 mM 3-isobutylmethylxanthine (Sigma), 1 mM dexamethasone (Sigma), 10 μg/mL insulin (Sigma) for 96 hours.…”

Section: T3-l1 Cell Culture and In Vitro Adipocyte Differentiationmentioning

confidence: 99%

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Lmo4‐resistin signaling contributes to adipose tissue‐liver crosstalk upon weight cycling

et al. 2020

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Repeated cycles of weight loss and regain, known as weight cycling, is often seen when people try to lose weight. The exact pathophysiological effects and the underlying mechanisms of weight cycling remain largely unclear. Here, we report that weight cycling induced by alternating feeding mice with a low‐fat diet or a high‐fat diet in a 1‐week switch protocol caused further increased epididymal white adipose tissue (eWAT) weight, preadipocyte proliferation, hepatic inflammation, fasting blood glucose level, and glucose intolerance, compared with the continuously HF‐fed mice. Combining the secretory protein database with RNA‐sequencing and quantitative PCR (qPCR) results in eWAT, the mRNA levels of several adipokines, including Retn (encoding resistin), were found altered by weight cycling. A transcriptional co‐factor Lmo4 was found regulated by weight cycling; Lmo4 enhanced preadipocyte proliferation, in vitro adipogenesis, transcription of Retn, and resistin secretion in 3T3‐L1 cells. Primary mouse hepatocytes administrated with recombinant mouse resistin (rm‐resistin), or exposed to media from Lmo4‐overexpressed 3T3‐L1 cells, showed increased inflammatory responses and gluconeogenesis. Furthermore, rm‐resistin‐injected normal chow‐fed mice showed upregulated blood glucose level by increasing gluconeogenesis, and upregulated the hepatic inflammatory responses. Together, our results suggest a regulatory role of Lmo4‐resistin signaling in weight cycling, indicating a crosstalk between the adipose tissue and liver.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: T3-l1 Cell Culture and In Vitro Adipocyte Differentiationmentioning

confidence: 99%

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Lmo4‐resistin signaling contributes to adipose tissue‐liver crosstalk upon weight cycling

et al. 2020

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“…Furthermore, we observed a drastic decrease of SLPI in the adipose tissue of the two patients. SLPI gene encodes a secretory leukocyte protease inhibitor, which is an important anti-inflammatory adipokine that counteracts adipose tissue inflammation and enhances browning of adipose tissue [25].…”

Section: Discussionmentioning

confidence: 99%

Unraveling LMNA Mutations in Metabolic Syndrome: Cellular Phenotype and Clinical Pitfalls

Desgrouas

Varlet

Dutour

et al. 2020

Cells

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This study details the clinical and cellular phenotypes associated with two missense heterozygous mutations in LMNA, c.1745G>T p.(Arg582Leu), and c.1892G>A p.(Gly631Asp), in two patients with early onset of diabetes mellitus, hypertriglyceridemia and non-alcoholic fatty liver disease. In these two patients, subcutaneous adipose tissue was persistent, at least on the abdomen, and the serum leptin level remained in the normal range. Cellular studies showed elevated nuclear anomalies, an accelerated senescence rate and a decrease of replication capacity in patient cells. In cellular models, the overexpression of mutated prelamin A phenocopied misshapen nuclei, while the partial reduction of lamin A expression in patient cells significantly improved nuclear morphology. Altogether, these results suggest a link between lamin A mutant expression and senescence associated phenotypes. Transcriptome analysis of the whole subcutaneous adipose tissue from the two patients and three controls, paired for age and sex using RNA sequencing, showed the up regulation of genes implicated in immunity and the down regulation of genes involved in development and cell differentiation in patient adipose tissue. Therefore, our results suggest that some mutations in LMNA are associated with severe metabolic phenotypes without subcutaneous lipoatrophy, and are associated with nuclear misshaping.

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“…A metabolic study was performed as previously described using a Comprehensive Lab Animal Monitoring System (CLAMS, Columbus Instruments, Columbus, OH). [ 27,28 ] O 2 consumption was measured for each mouse over 3 days. Mice were allowed to acclimate to the environment for 24 h and the average of day 2 and 3 was reported.…”

Section: Methodsmentioning

confidence: 99%

Vitamin C Inhibits the Metabolic Changes Induced by Tet1 Insufficiency Under High Fat Diet Stress

Yuan

Liu

Chen

et al. 2021

Molecular Nutrition Food Res

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Scope DNA methylation contributes to obesity, but the role of the DNA demethylase ten‐eleven translocation protein 1 (Tet1) in obesity remains unclear. Vitamin C is a cofactor for the Tet family of proteins, but whether vitamin C can be used to treat obesity via Tet1 awaits clarification. Methods and Results Tet1+/+ and Tet1+/− mice are fed a high fat diet (HFD). Higher weight gain and more severe hepatic steatosis, accompanied by reduced 5‐hydromethylcytosine (5hmC) levels, are found in the white adipose tissue and liver of Tet1+/− mice. Accumulated lipids are observed in palmitic acid or oleic acid treated primary hepatocytes derived from Tet1+/− mice, which are rescued by Tet1 overexpression or vitamin C treatment. Bisulfite sequencing reveals higher DNA methylation levels on lipolysis related genes in the liver of Tet1+/− mice. Notably, oral intake of vitamin C normalizes DNA methylation levels, promotes lipolysis, and decreases obesity in HFD‐fed Tet1+/− mice. Conclusions The results reveal a novel function of Tet1 in obesity and provide a new mechanism for the beneficial role of vitamin C in metabolic diseases through enhanced Tet1 activity.

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Fat-Specific Knockout of Mecp2 Upregulates Slpi to Reduce Obesity by Enhancing Browning

Cited by 30 publications

References 48 publications

Lmo4‐resistin signaling contributes to adipose tissue‐liver crosstalk upon weight cycling

Lmo4‐resistin signaling contributes to adipose tissue‐liver crosstalk upon weight cycling

Unraveling LMNA Mutations in Metabolic Syndrome: Cellular Phenotype and Clinical Pitfalls

Vitamin C Inhibits the Metabolic Changes Induced by Tet1 Insufficiency Under High Fat Diet Stress

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