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OBJECTIVE To explore the mechanism of Yishen tongluo formula （YSTLF） in improving abnormal lipid metabolism based on the sterol regulatory element binding proteins （SREBPs） pathway. METHODS Using C57BLKS/J （db/db） mice as model and C57BLKS/J （db/m） mice as normal control， the mechanism of 1， 2.5 and 5 g/kg YSTLF improving abnormal lipid metabolism of db/db mice was investigated by determining the liver coefficient， the contents of serum total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein （LDL） and high-density lipoprotein （HDL）， observing steatosis and lipid accumulation in liver tissue of mice， detecting the protein expressions of SREBP-1 and SREBP-2 as well as mRNA transcription levels of Srebp- 1c， Srebp-2 and their downstream lipid metabolism-related target genes （Fasn， Acc1， Scd5， Fads1， Hmgcr， Dhcr24， Insig-1， Fdps） in liver tissue of mice. Using low-fat cultured human liver cancer cell HepG2 as an in vitro cell model for abnormal lipid metabolism， and 25-HC （SREBPs inhibitor， 10 μmol/L） as the control， the effects of 125， 250 and 500 μg/mL YSTLF on protein expressions of SREBP-1 and SREBP-2 as well as mRNA transcription of SREBP-1c， SREBP-2 and their downstream lipid metabolism-related target genes were investigated to verify the mechanism in vitro. RESULTS 1， 2.5， 5 g/kg YSTLF significantly reduced the levels of TC， TG and LDL， the percentage of lipid droplet-positive region in liver tissue and liver coefficient， significantly down-regulated protein expressions of Pre-SREBP-1， n-SREBP-1， Pre-SREBP-2 and n-SREBP-2， and mRNA transcription of Srebp-1c， Srebp-2 and their downstream target genes in liver tissue， while significantly increased HDL level， with statistical significance （P＜0.05 or P＜0.01）. In the cell experiment in vitro， the expressions of the above-mentioned proteins and genes in the cells treated with YSTLF at 125， 250 and 500 μg/mL for 24 hours were consistent with those in the animal experiment； there was no significant difference in the expressions of the above-mentioned proteins and genes between inhibitor control group and 250， 500 μg/mL YSTLF groups （P＞0.05）. CONCLUSIONS YSTLF can regulate the expression of transcription factor SREBPs， so as to inhibit the high expression of fatty acid and cholesterol synthesis-related genes， promote the degradation of TC and TG， improve the abnormality of lipid metabolism and inhibit lipid accumulation， thus playing the role of lipid-lowering.
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To address the issue of weight gain and abnormal lipid metabolism caused by clozapine and olanzapine administration in patients with schizophrenia， a qualitative and systematic review was carried out， thus providing references for clinical treatment and future research. This review embraces the aspects of pharmacotherapy， traditional Chinese medicine treatment and so on.
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Congenital generalized lipodystrophy type 1 (CGL1) is an autosomal recessive genetic disease caused by mutations in AGPAT2 gene. The main clinical mainifestations include body subcutaneous fat loss, muscle hypertrophy, obvious subcutaneous veins, pseudoacromegaly, hirsutism, and acanthosis nigricans. What′s more, CGL1 is always accompanied by metabolic diseases. Therefore, it is easily misdiagnosed as metabolic syndrome, type 2 diabetes, polycystic ovary syndrome, acromegaly, or Cushing′s syndrome. Meanwhile, it is difficult to distinguish it from partial lipoatrophy syndrome. In this article, we present clinical and molecular characteristics of a patient with CGL1 and review mutations reported in literature to replenish current knowledge about this orphan disease.
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Objective To explore the correlation between homocysteine(Hcy),lipids amd type 2 diabetes mellitus (T2DM). Methods The laboratory test results of 533 cases of patients with T2DM(T2DM group)and 362 cases of healthy individuals (healthy control group)were retrospectively analyzed.Results The serum levels of Hcy and rates of abnormal serum cholesterol (TC),triacylglycerol(TG),low density lipoprotein cholesterol(LDL-C),high density lipoprotein cholesterol(HDL-C)levels in the T2DM group were higher than those in the healthy control group,had statistically significant differences(P <0.05).Conclusion The high serum level of Hcy and abnormal lipid metabolism are correlated with T2DM,which might be risk factors of diabetes mel-litus and cardiovascular disease.
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@#Both dysfunction of pancreatic β cells and β cells apoptosis were important factors contributing to type 2 diabetes. Abnormal glucose and lipid metabolism all existed in type 2 diabetes .With the study further progressing, more and more attention were paid to pancreatic β cells apoptosis accelerated by abnormal lipid metabolism. The literature about β cells injury by lipotoxicity, apoptosis induced factors accompanied by free fatty acids, and relevant mechanism was reviewed in this article.
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In this paper,we study on turbidity-toxin from the connotation,the pathological characteristics and process of diabetes,and explored the relationship of type 2diabetes with abnormal lipid metabolism and lipid toxicity.We found that insulin resistance,apoptosis of Islet,cell and various complications caused by abnormal lipid metabolism and lipid toxicity had signifi cant correlation with the process of the generation and variation of turbidity-toxin:it was argued that blood turbidity and its subsequent toxin accumulation were the pathogenic basis of the formation,combing with the turbidity-toxin,phlegm and blood stasis,then various complications occurred.So it provided a good theoretical and practical foundation for further treatment of type 2 diabetes associated with abnormal lipid metabolism by removing turbidity and detoxication.