Inflammatory and Metabolic Influences on Osteoarthritis by High-Fat Diet in Mice
學生姓名:
龍秉廷
指導教授:
龔瑞林
學 號:
10332017
學期:
104上
摘 要:
Osteoarthritis (OA) is a painful and debilitating disease of the synovial joints and is characterized by degeneration and inflammation of the articular cartilage and other joint tissue. Except degeneration with age one of the common conditions that lead to OA is obesity. Adipose tissue recently is recognized as playing a role in many diseases through secretion of adipose-derived cytokines (i.e., “adipokines”) and hormones, resulting in chronic low-grade systemic inflammation. The aim of this study is what reason caused obesity-induced osteoarthritis.
First the study was to investigate the role of high-density lipoprotein (HDL) metabolism in the pathobiology of OA. The results showed HDL metabolism related apolipoprotein A-I (apoA-I) and lecithin: cholesterol acyltransferase (LCAT) deficiency lead to OA condition following with Western-type diet (WTD). Secondly, a study examines the interrelationships between joint degeneration and serum levels of the inflammatory cytokines and adipokines that are involved in this response. Results suggested that diet-induced obesity significantly increases the severity of OA following intra articular fracture. Obesity and joint injury together can alter systemic levels of inflammatory cytokines such as IL-12p70. Thirdly, another study to test the hypothesis that metabolic stress-induced inflammation, not mechanical overload, is responsible for the development of high-fat diet-induced OA in mice. The resultant high-fat diet-induced OA was due to low-grade inflammation and using statins or peroxisome proliferator-activated receptor γ agonists shall decrease progression of OA.
In conclusion, high fat diet-induced osteoarthritis could increase cartilage degradation and synovial inflammation of the fractured limb, decreased “whole joint” posttraumatic arthritis. The mechanism of HDL relative LCAT enzyme and ApoA-I protein plays a major role in the development of osteoarthritis. Furthermore, the article verified Statins and peroxisome proliferator-activated receptor γ agonist decreased inflammatory osteoarthritis.
First the study was to investigate the role of high-density lipoprotein (HDL) metabolism in the pathobiology of OA. The results showed HDL metabolism related apolipoprotein A-I (apoA-I) and lecithin: cholesterol acyltransferase (LCAT) deficiency lead to OA condition following with Western-type diet (WTD). Secondly, a study examines the interrelationships between joint degeneration and serum levels of the inflammatory cytokines and adipokines that are involved in this response. Results suggested that diet-induced obesity significantly increases the severity of OA following intra articular fracture. Obesity and joint injury together can alter systemic levels of inflammatory cytokines such as IL-12p70. Thirdly, another study to test the hypothesis that metabolic stress-induced inflammation, not mechanical overload, is responsible for the development of high-fat diet-induced OA in mice. The resultant high-fat diet-induced OA was due to low-grade inflammation and using statins or peroxisome proliferator-activated receptor γ agonists shall decrease progression of OA.
In conclusion, high fat diet-induced osteoarthritis could increase cartilage degradation and synovial inflammation of the fractured limb, decreased “whole joint” posttraumatic arthritis. The mechanism of HDL relative LCAT enzyme and ApoA-I protein plays a major role in the development of osteoarthritis. Furthermore, the article verified Statins and peroxisome proliferator-activated receptor γ agonist decreased inflammatory osteoarthritis.
10332017-3-龍秉廷-龔瑞林.pdf