Abstract | OBJECTIVE: To investigate the effects of catch-up growth (CUG) on the natch domain, leucine-rich repeat and PVD-containing protein 3 (NALP3) inflammasome pathway in visceral adipose tissue (VAT) and the mechanism of insulin resistance (IR) in CUG. METHODS: Sprague-Dawley rats were randomly divided into the normal chow (NC) and the catch-up growth group (CUG). General characteristics, glucose infusion rate60-120 (GIR60-120) in hyperinsulinemic-euglycemic clamp and expression of NALP3 inflammasome, caspase1(p10) and IL-1β (p17) cleavage in VAT were respectively examined on week 4, 6 and 8 of the experiment. RESULTS: After 4-week food restriction, lower percentage of abdominal fat mass (AFM%) was presented in the CUG group than the NC group [(11.54 ± 1.81)% vs (7.72 ± 1.47)%, P < 0.05]. In the CUG group, decreased expression of NALP3 inflammasome, caspase1 (p10) and IL-1β (p17) cleavage in VAT were found (0.47 ± 0.03 vs 0.28 ± 0.04, P < 0.01; 0.30 ± 0.02 vs 0.20 ± 0.03, P < 0.01; 0.52 ± 0.04 vs 0.37 ± 0.04, P < 0.05; respectively), whereas GIR60-120 was slightly improved [(23.47 ± 0.89) mg×min(-1)×kg(-1) vs (25.34 ± 1.16) mg×min(-1)×kg(-1), P > 0.05]. After refeeding, AFM% and the expression of NALP3 inflammasome, caspase1 (p10) and IL-1β (p17) cleavage in VAT in CUG group were shown to be increased with the time. Concomitant with those changes, GIR60-120 was gradually impaired. On week 4 of refeeding, AFM% and the expression of NALP3 inflammasome, caspase1 (p10) and IL-1β (p17) cleavage in VAT were significantly increased in the CUG group compared with the NC group [(12.52 ± 0.64)% vs (15.16 ± 1.10)%, P < 0.01; 0.52 ± 0.02 vs 0.65 ± 0.05, P < 0.05; 0.33 ± 0.03 vs 0.54 ± 0.02, P < 0.01; 0.55 ± 0.04 vs 0.65 ± 0.05, P < 0.05; respectively], while GIR60-120 was significantly attenuated [(21.45 ± 1.20) mg×min(-1)×kg(-1) vs (14.27 ± 1.06) mg×min(-1)×kg(-1), P < 0.05]. Correlation analysis showed that the expression of NALP3 and caspase1 (p10) in VAT were positively correlated with AFM% (r = 0.946, P < 0.01; r = 0.922, P < 0.01), while negatively correlated with GIR60-120 (r = -0.902, P < 0.01; r = -0.944, P < 0.01). CONCLUSION: NALP3 inflammasome pathway in VAT is notably activated during CUG, which may contribute to the etiology of IR in CUG.
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Authors | Yan Li, Lulu Chen, Xiang Hu, Shan Yu, Juan Zheng, Huiqing Li, Tianshu Zeng, Wenfang Xia, Jiaoyue Zhang |
Journal | Zhonghua nei ke za zhi
(Zhonghua Nei Ke Za Zhi)
Vol. 53
Issue 6
Pg. 482-6
(Jun 2014)
ISSN: 0578-1426 [Print] China |
PMID | 25146519
(Publication Type: Journal Article)
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Chemical References |
- Carrier Proteins
- Inflammasomes
- Interleukin-1beta
- NLR Family, Pyrin Domain-Containing 3 Protein
- Nlrp3 protein, rat
- Receptors, Cytoplasmic and Nuclear
- Glucose
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Topics |
- Animals
- Carrier Proteins
- Glucose
- Inflammasomes
- Insulin Resistance
- Interleukin-1beta
- Intra-Abdominal Fat
(metabolism)
- NLR Family, Pyrin Domain-Containing 3 Protein
- Rats
- Rats, Sprague-Dawley
- Receptors, Cytoplasmic and Nuclear
(physiology)
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