Hyperlipidemia, type 2 diabetes mellitus, nonalcoholic fatty liver and many other metabolic disorder are frequently co-existing in patients. In addition, these diseases are closely related in pathophysiological settings. However, increasing of the disease incidence, lacking of comprehensive prevention and control measurements against the key pathology point concomitant occurrence with the pattem of the single disease, single target therapy, that is leading therapeutic strategy for these metabolic disorders in the setting of Western medicine （WM）. On the basis of the combination of the advantages of integrated Chinese medicine （CM） and WM, with unified understanding of such diseases, the new concept of glucolipid metabolic disease （GLMD） is introduced. In this new concept, disorders in glucose and lipid metabolism are recognized as the key trigger and major driving force for the progress of GLMD. The key points of pathology included dysfunction of neuronal-endocrine-immune system,insulin resistance, oxidative stress, inflammation and intestinal flora imbalance. In the core pathogenic perspective of CM, it can be explained as ＂Gan （Liver） Shi Shu Xie＂ （dysfunction of Gan in metabolism and emotion regulation） that will lead to the occurence/production of endogenous dampness and phlegm, blood stasis and turbid. This leads to the new concept of ＂Liver-based regulatory system for metabolic homeostasis＂ to be introduced further. The comprehensive prevention and control strategy ＂Tiao Gan Qi Shu Hua Zhuo＂ （modulating Gan, trigging key metabolic system to resolve pathogenic factors such as phlegm retention and dampness）. Its representative formula Fufang Zhenzhu Tiaozhi Capsule （复方贞术调脂胶囊） is innovated under such rationales. Comment for some commonly-used CM GLMD therapeutic drugs was presented. High-level evidence-based and epidemiological and mechanism studies should be carded out to further interpret and explain of the scientific connotation of GLMD.
Objective： To investigate the protective effects of Chinese medicine formulation Chaihu Shugan San（柴胡疏肝散, CHSGS） on nonalcoholic fatty liver disease（NAFLD） in rats with insulin resistance（IR） and its molecular mechanisms. Methods： Male Sprague-Dawley rats were randomly divided into six groups： the control group, the model group, Dongbao Gantai group（东宝肝泰, DBGT, 0.09 g methionine/kg）, CHSGS high-dose group（CHSG-H, 12.6 g crude drug/kg）, CHSGS medium-dose group（CHSG-M, 6.3 g crude drug/kg）, and CHSGS low-dose group（CHSG-L, 3.15 g crude drug/kg）. After establishing the NAFLD rat model and treatment for 8 weeks, total cholesterol（TC）, triglyceride（TG）, high-density lipoprotein cholesterol（HDL-C）, free fatty acid（FFA）, fasting blood glucose（FBG）, fasting insulin（FINS） contents in blood serum, and TC, TG contents in the hepatic homogenate were measured by an automatic biochemical analyzer, and a homeostasis model assessment was applied to assess the status of IR, insulin sensitivity index（ISI）, and homeostasis model assessment for insulin secretion（HOMA-IS）. The expression levels of adiponectin and leptin mRNA in liver tissue were analyzed by reverse transcription polymerase chain reaction. Pathological changes of livers were observed by hematoxylineosin staining of paraffin section. Results： Compared with the model group, the serum levels of TC, TG, FFA, FBG, FINS, IRI, ISI, and the liver levels of TC and TG in CHSG-H, CHSG-M, CHSG-L groups showed significant declines（P〈0.01 or P〈0.05）; the serum levels of HDL-C, HOMA-IS were significantly increased（P〈0.01 or P〈0.05）; the expression of leptin mRNA was dramatically decreased and the expression of adiponectin mRNA was increased in the hepatic tissue（P〈0.01 or P〈0.05）. The fatty deposition of liver cells could also be alleviated. Conclusion： CHSGS could up-regulate the expression of adiponectin mRNA and down-regulate the expression of leptin mRNA on the liver,
