Role of Peroxisome Proliferator‐Activated Receptor (PPARγ) in Metabolic Disorders in SGA with Catch‐Up Growth

Lian, Qiong-Xia; Deng, Hong-zhu; Chen, Kaiyun; Deng, Hong

doi:10.1002/oby.22030

Cited by 3 publications

(5 citation statements)

References 33 publications

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“…Additionally, PGC-1α is also a coactivator of various transcription factors expressed in skeletal muscle, including PPARγ [ 27 ]. Lian et al have reported that SGA individuals may exhibit high PPARγ expression, which may lead to abnormal fatty acidosis and lipid metabolism disorders [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth

et al. 2022

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Background Studies have shown that the high incidence of type 2 diabetes in China is associated with low birth weight and excessive nutrition in adulthood, which occurred during the famine years of the 1950s and 1960s, though the specific molecular mechanisms are unclear. In this study, we proposed a severe maternal caloric restriction during late pregnancy, followed by a post weaning high-fat diet in mice. After weaning, normal and high-fat diets were provided to mice to simulate the dietary pattern of modern society. Methods The pregnant mice were divided into two groups: normal birth weight (NBW) group and low birth weight (LBW) group. After 3 weeks for weaning, the male offspring mice in the NBW and LBW groups were then randomly divided into four subgroups: NC, NH, LC and LC groups. The offspring mice in the NC, NH, LC and LC groups were respectively fed with normal diet, normal diet, high-fat diet and high-fat diet for 18 weeks. After 18 weeks of dietary intervention, detailed analyses of mRNA and protein expression patterns, signaling pathway activities, and promoter methylation states were conducted for all relevant genes. Results After dietary intervention for 18 weeks, the expressions of CD36, Fabp4, PPARγ, FAS, and ACC1 in the skeletal muscle tissue of the LH group were significantly increased compared with the LC and NH groups (P < 0.05). The level of p-AMPK/AMPK in the skeletal muscle tissue of the LH group was significantly decreased compared with the LC and NH groups (P < 0.05). CPT1 and PGC-1α protein expressions were up-regulated in the LH group (P < 0.05) compared to the LC group. Additionally, the DNA methylation levels of the PGC-1α and GLUT4 gene promoters in the skeletal muscle of the LH groups were higher than those of the LC and NH groups (P < 0.05). However, PPARγ DNA methylation level in the LH group was lower than those of the LC and NH groups (P < 0.05). Conclusions LBW combined with high-fat diets may increase insulin resistance and diabetes through regulating the CD36-related Fabp4-PPARγ and AMPK/ACC signaling pathways.

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Section: Discussionmentioning

confidence: 99%

The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth

et al. 2022

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“…Body weight and length were measured weekly. CUG-SGA rats were identified when the body weight and body length were –2 SD higher than those in the control group at 4 weeks of age ( 11 , 20 , 21 ).…”

Section: Methodsmentioning

confidence: 99%

“…Children born SGA with CUG have been reported to have fat accumulation, abnormal adipocyte function, and development of adipose tissue caused by adverse intrauterine growth ( 8 , 9 ). Excess fat accumulation can lead to free fatty acid (FFA) release, and high concentrations of FFA can induce insulin resistance in the muscle and liver ( 10 , 11 ). Thus, to develop strategies to prevent insulin resistance, it is crucial to understand the relative contribution of CUG to the emergence of the condition.…”

Section: Introductionmentioning

confidence: 99%

Adipose tissue macrophage-derived exosomal miR-210-5p in modulating insulin sensitivity in rats born small for gestational age with catch-up growth

Xiong¹,

Liu²,

Song³

et al. 2023

Transl Pediatr

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Background: Insulin resistance has been implicated in the pathogenesis of children born small for gestational age (SGA) with catch-up growth (CUG). Adipose tissue macrophages (ATMs) regulate insulin resistance by secreting exosomes containing microRNA (miRNA) cargo; however, their pathogenic roles and molecular mechanism are not fully understood. This study aimed to investigate the role of miR-210-5p in rats born SGA with CUG and insulin resistance. Methods:The dietary needs of pregnant rats were restricted to ensure the birth of SGA rats. Transmission electron microscopy (TEM) and Western blot analysis were used to identify the exosomes from ATMs of CUG-SGA and adequate-for-gestational-age (AGA) rats. PKH-67 staining was performed to confirm the uptake of exosomes. miR-210-5p expression was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Glucose uptake and output were detected with glucose uptake and output assays, respectively. Insulin resistance was detected with glucose and insulin tolerance tests in vivo. The interaction between miR-210-5p and SID1 transmembrane family member 2 (SIDT2) was validated with dual-luciferase reporter assay.Results: miR-210-5p was observed to be highly expressed in the exosomes derived from the ATMs of CUG-SGA rats. ATM-derived exosomes can serve as vehicles to deliver miR-210-5p into adipocytes, myocytes, and hepatocytes, where it can enhance cellular insulin resistance. SIDT2 was identified as a direct target gene of miR-210-5p. The miR-210-5p-induced insulin resistance was reversed by the restored SIDT2 expression. However, overexpression of SIDT2 abolished the inhibitory effect of CUG-SGA-ATM-exosomal miR-210-5p on insulin sensitivity in vivo.Conclusions: ATM-derived exosomal miR-210-5p promoted insulin resistance in CUG-SGA rats by targeting SIDT2, which may act as a new potential therapeutic target for children born SGA with CUG.

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“…PPAR-γ is fundamental in adipogenesis and adipocyte differentiation, accumulating several functions [ 7 , 9 , 10 ]. This receptor is involved in the process of lipid signaling, which allows lipids to be transported from metabolic organs, including the liver and skeletal muscle, to white adipose tissue (WAT) [ 7 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, it modulates the expression of adipokines to promote adipocyte differentiation, specifically by increasing the expression of adiponectin and decreasing leptin expression [ 7 , 10 , 11 ]. Furthermore, this transcription factor is involved in cholesterol and triglyceride plasma regulation, which indirectly relates to cardiovascular comorbidities such as atherogenesis and coronary heart disease [ 9 ]. Additionally, PPAR-γ regulates the inflammation observed in WAT, not only by polarizing M1 macrophages, but also by reducing the concentration of these cell types [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Enhanced 3T3-L1 Differentiation into Adipocytes by Pioglitazone Pharmacological Activation of Peroxisome Proliferator Activated Receptor-Gamma (PPAR-γ)

Teixeira

Sousa

Santos

et al. 2022

Biology

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Despite the primary function of pioglitazone in antidiabetic treatment, this drug is a potent inducer of PPAR-γ, a crucial receptor that is involved in adipocyte differentiation. In this work, we propose an optimized methodology to enhance the differentiation of 3T3-L1 fibroblasts into adipocytes. This process is crucial for adipocyte secretome release, which is fundamental for understanding the molecular mechanisms that are involved in obesity for in vitro studies. To achieve this, a pioglitazone dose-response assay was determined over a range varying from 0 to 10 µM. Lipid accumulation was evaluated using Oil-Red-O. The results showed that 10 µM pioglitazone enhanced differentiation and increased secretome production. This secretome was then added into two cell lines: PC3 and RAW264.7. In the PC3 cells, an increase of aggressiveness was observed in terms of viability and proliferation, with the increase of anti-inflammatory cytokines. Conversely, in RAW264.7 cells, a reduction of viability and proliferation was observed, with a decrease in the overexpression of pro-inflammatory cytokines. Overall, the present work constitutes an improved method for adipocyte secretome production that is suitable for experimental biology studies and that could help with our understanding of the molecular mechanisms underlying adiposity influence in other cells.

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Role of Peroxisome Proliferator‐Activated Receptor (PPARγ) in Metabolic Disorders in SGA with Catch‐Up Growth

Cited by 3 publications

References 33 publications

The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth

The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth

Adipose tissue macrophage-derived exosomal miR-210-5p in modulating insulin sensitivity in rats born small for gestational age with catch-up growth

Enhanced 3T3-L1 Differentiation into Adipocytes by Pioglitazone Pharmacological Activation of Peroxisome Proliferator Activated Receptor-Gamma (PPAR-γ)

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