scholarly journals Effect of Curcumin on Growth Performance, Inflammation, Insulin level, and Lipid Metabolism in Weaned Piglets with IUGR

Animals ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 1098 ◽  
Author(s):  
Yu Niu ◽  
Jintian He ◽  
Yongwei Zhao ◽  
Mingming Shen ◽  
Lili Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Slow Growth ◽  
Hepatic Glycogen ◽  
Lipid Levels ◽  
Weaned Piglets ◽  
Hepatic Lipid ◽  
Pro Inflammatory Cytokines

The possible causes of intrauterine growth retardation (IUGR) might stem from placental insufficiency, maternal malnutrition, inflammation in utero, and other causes. IUGR has had an adverse influence on human health and animal production. Forty weaned piglets with normal birth weights (NBWs) or IUGR were randomly divided into four treatments groups: NBW, NC (NBW with curcumin supplementation), IUGR, and IC (IUGR with curcumin supplementation) from 26 to 50 d. Levels of cytokines, glucose, and lipid metabolism were evaluated. IUGR piglets showed slow growth during the experiment. Piglets with IUGR showed higher levels of serum pro-inflammatory cytokines, insulin resistance, and hepatic lipid accumulation. Curcumin supplementation reduced the production of serum pro-inflammatory cytokines, attenuated insulin resistance and hepatic triglyceride, and enhanced the hepatic glycogen concentrations and lipase activities of IUGR piglets. The hepatic mRNA expressions of the insulin-signaling pathway and lipogenic pathway were influenced by IUGR and were positively attenuated by diets supplemented with curcumin. In conclusion, IUGR caused slow growth, insulin resistance, and increased hepatic lipid levels. Diets supplemented with curcumin improved growth, attenuated insulin resistance, and reduced lipid levels in the liver by regulating the hepatic gene expressions of the related signaling pathway in IUGR piglets.

scholarly journals Effects of Distinct n-6 to n-3 Polyunsaturated Fatty Acid Rations on Insulin Resistant and AD-like Phenotypes in High-Fat Diets-Fed APP/PS1 Transgenic Mice

2021 ◽  
Author(s):  
Xiaojun Ma ◽  
Yujie Guo ◽  
Pengfei Li ◽  
Jingjing Xu ◽  
Shengqi Dong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
High Fat ◽  
Pufa Ratio ◽  
Pro Inflammatory Cytokines

Abstract Background: Type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) are two prevalent diseases with comparable pathophysiological features and genetic predisposition. Polyunsaturated fatty acids (PUFAs) are essential in maintaining normal brain function. However, little is known about the impact of dietary n-6/n-3 PUFA ratio on AD-like pathology, especially in high-fat diet (HFD)-fed AD model mice. Methods: In the present study, the APP/PS1 mice were treated with 60% HFD for 3.5 months to induced insulin resistance. After that, 45% HFD with different n-6/n-3 PUFA ratios (n-6/n-3=1:1, 5:1 or 16:1) was applied for additional 3.5 months treatment. Following the dietary intervention, the behavior of mice was observed using the Water maze. Following behavioral testing, the animals were euthanized, and serum and tissue samples were collected for biochemical, histological and pathological analyses and evaluation. Cortical fatty acid profile was measured by gas chromatography. Western Blot and immunohistochemistry methods were used to detect protein expression of molecules related to AD pathology and insulin signaling pathway(s) in the brain sample tissues. Immunofluorescence assay was used to uncover the expression and migration of NF-κB in the cortex. qPCR method was applied to determine the gene expression of cortical pro-inflammatory cytokines.Results: HFD caused insulin resistance, increased serum IL-6 and TNF-α level, elevated cortical soluble Aβ1-40, Aβ1-42 content, and increased brain n-6/n-3 PUFAs ratio in APP/PS1 mice. Increased APP and BACE1 protein expression and p-IR/IR ratio, but decreased pro-inflammatory cytokines mRNA expression was observed in the cortex from 60% HFD-fed APP/PS1 mice. N-3 PUFAs rich diet (n-6/n-3=1:1) relieved insulin resistance and hyperlipidemia induced by 60% HFD. Cortical soluble Aβ1-40 and Aβ1-42 contents, the expression of cortical APP, GLUT3, insulin metabolism related molecules, and NF-κB pathway downstream pro-inflammatory cytokines showed a dietary n-6/n-3 PUFAs ratio-dependent way, indicating that dietary n-6/n-3 PUFA ratio plays a critical role in modifying the responses of serum inflammatory cytokine, AD pathology, cortical n-6/n-3 PUFAs ratio, insulin signaling and neuroinflammation to HFD treatment.Conclusion: Dietary n-6/n-3 PUFA ratio play an important role in modifying AD pathophysiology, insulin signaling pathway, and neuro-inflammation response to high fat diet treatment in brain.

scholarly journals Abdominal Massage Alleviates Skeletal Muscle Insulin Resistance by Regulating the AMPK/SIRT1/PGC-1α Signaling Pathway

2021 ◽  
Author(s):  
Yiran Han ◽  
Zeyuan Lu ◽  
Shaotao Chen ◽  
Chongwen Zhong ◽  
Minghui Yan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
High Fat ◽  
Abdominal Massage ◽  
Pro Inflammatory Cytokines

AbstractAbdominal massage (AM), a traditional Chinese medicine-based treatment method, has received considerable attention in the recent years. The aim of the present study was to investigate the effect of AM on high-fat diet (HFD)-induced insulin resistance (IR) in comparison with resveratrol (RSV) treatment. Forty-eight male Sprague-Dawley rats were randomly divided into the following four groups: standard chow diet (control group), high-fat diet (model group), HFD + abdominal massage (AM group), and HFD + resveratrol (RSV group). A rat model of IR was established by feeding HFD to rats for 8 weeks followed by treatment with AM or RSV for 4 weeks. The underlying HFD-induced IR molecular mechanisms were studied in rat serum and skeletal muscles. RSV and AM significantly improved glucose intolerance, hyperglycemia, obesity, and significantly reduced lipid accumulation [triglyceride (TC), total cholesterol (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)], adipocytokine [free fatty acids (FFA), adiponectin (ADPN)] and serum pro-inflammatory cytokines (IL-6 and TNF-α) secretion. In addition, AM activated the AMPK/SIRT1 signaling pathway in rat skeletal muscle. In conclusion, our results showed that AM could improve IR by regulating the secretion of adipocytokines, pro-inflammatory cytokines as well as related signaling pathways in the skeletal muscle of rats, which might provide insights into development of new treatment methods for the clinical treatment of IR.

scholarly journals Punicalagin Prevents Inflammation in LPS-Induced RAW264.7 Macrophages by Inhibiting FoxO3a/Autophagy Signaling Pathway

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2794 ◽  
Author(s):  
Cao ◽  
Chen ◽  
Ren ◽  
Zhang ◽  
Tan ◽  
...  
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Inflammatory Responses ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Autophagy Inhibition ◽  
Pro Inflammatory Cytokines

Punicalagin, a hydrolysable tannin of pomegranate juice, exhibits multiple biological effects, including inhibiting production of pro-inflammatory cytokines in macrophages. Autophagy, an intracellular self-digestion process, has been recently shown to regulate inflammatory responses. In this study, we investigated the anti-inflammatory potential of punicalagin in lipopolysaccharide (LPS) induced RAW264.7 macrophages and uncovered the underlying mechanisms. Punicalagin significantly attenuated, in a concentration-dependent manner, LPS-induced release of NO and decreased pro-inflammatory cytokines TNF-α and IL-6 release at the highest concentration. We found that punicalagin inhibited NF-κB and MAPK activation in LPS-induced RAW264.7 macrophages. Western blot analysis revealed that punicalagin pre-treatment enhanced LC3II, p62 expression, and decreased Beclin1 expression in LPS-induced macrophages. MDC assays were used to determine the autophagic process and the results worked in concert with Western blot analysis. In addition, our observations indicated that LPS-induced releases of NO, TNF-α, and IL-6 were attenuated by treatment with autophagy inhibitor chloroquine, suggesting that autophagy inhibition participated in anti-inflammatory effect. We also found that punicalagin downregulated FoxO3a expression, resulting in autophagy inhibition. Overall these results suggested that punicalagin played an important role in the attenuation of LPS-induced inflammatory responses in RAW264.7 macrophages and that the mechanisms involved downregulation of the FoxO3a/autophagy signaling pathway.

scholarly journals Pycnogenol protects against diet-induced hepatic steatosis in apolipoprotein-E-deficient mice

2018 ◽  
Vol 315 (2) ◽  
pp. E218-E228 ◽  
Author(s):  
Difei Wang ◽  
Huiying Cong ◽  
Xiaoli Wang ◽  
Yanli Cao ◽  
Shoichiro Ikuyama ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Apolipoprotein E ◽  
Hepatic Steatosis ◽  
Inflammatory Cytokines ◽  
Lipid Content ◽  
Acid Uptake ◽  
Short Term Treatment ◽  
Hepatic Lipid ◽  
Deficient Mice ◽  
Hepatic Lipid Content

PycnogenolR (PYC), a combination of active flavonoids derived from French maritime pine bark, is a natural antioxidant that has various pharmacological activities. Here, we investigated the beneficial effect of PYC on diet-induced hepatic steatosis. Apolipoprotein E (ApoE)-deficient male mice were administered PYC at oral doses of 30 or 100 mg·kg−1·day−1 for 2 wk in advance and were then fed a high-cholesterol and -fat diet (HCD) for 8 wk. Biochemical, immunohistochemical, and gene expression analyses were conducted to explore the effect of PYC on lipid metabolism in ApoE-deficient mice on a HCD. Short-term treatment with HCD in ApoE-deficient mice induced hepatic injuries, such as lipid metabolism disorder and hepatic histopathological changes. We found that PYC reduced body weight and the increase of serum lipids that had been caused by HCD. Supplementation of PYC significantly reduced lipid deposition in the liver, as shown by the lowered hepatic lipid content and histopathological lesions. We subsequently detected genes related to lipid metabolism and inflammatory cytokines. The study showed that PYC markedly suppressed the expression of genes related to hepatic lipogenesis, fatty acid uptake, and lipid storage while increasing the lipolytic gene, which thus reduced hepatic lipid content. Furthermore, PYC mainly reduced the expression of inflammatory cytokines and the infiltration of inflammatory cells, which were resistant to the development of hepatic steatosis. These results demonstrate that PYC protects against the occurrence and development of hepatic steatosis and may provide a new prophylactic approach for nonalcoholic fatty liver disease (NAFLD).

scholarly journals Maternal conjugated linoleic acid alters hepatic lipid metabolism via the AMPK signaling pathway in chick embryos

2020 ◽  
Vol 99 (1) ◽  
pp. 224-234
Author(s):  
Chunyan Fu ◽  
Yan Zhang ◽  
Qimeng Yao ◽  
Xiangfa Wei ◽  
Tianhong Shi ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Signaling Pathway ◽  
Chick Embryos ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid ◽  
Ampk Signaling

scholarly journals Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway

2019 ◽  
Vol 25 (12) ◽  
pp. 1492-1501 ◽  
Author(s):  
Jie Hu ◽  
Wei Hong ◽  
Kan-Nan Yao ◽  
Xiao-Hong Zhu ◽  
Zhi-Yun Chen ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Ursodeoxycholic Acid ◽  
Signaling Pathway ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid
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