In the endoplasmic reticulum (ER), nascent glycoproteins are folded by calnexin/calreticulin (CNX/CRT) cycle related lectins and enzymes. The folding cycle is mainly regulated by CNX, CRT, glucosidase II (GII) and UDP-glucose: glycoprotein glucosyltransferase (UGGT). Misfolding of glycoproteins have been known to induce ER stress. Since excessive ER stress causes folding diseases represented by diabetes mellitus, operating status of the cycle is very significant. In this study, we examined relevance between metabolic syndrome rat model livers and the operating status focused on transcription, expression and activity of the cycle related lectins and enzymes. In obesity rat model livers, all cycle related proteins were decreased in transcription, expression and activity than healthy rat model livers. The results indicate function of CNX/CRT cycle has declined in obesity rat model. Also these observations indicate mRNA/protein expression levels and activity were correlated in obesity rat liver. In severe diabetes, transcription levels of CNX and GII were increased than obesity rat model. On the other hand, the levels of CRT and UGGT were not changed. In expression level, similar tendency was observed. In contrast, activity of cycle related proteins were varied. Namely, activities of CNX and CRT were increased than obesity rat liver. Activity of GII was not changed compare to obesity rat liver. Activity of UGGT was decreased rather than obesity rat liver. These results indicate mRNA/protein expression levels and activity were not correlated in diabetes rat liver. In view of misfolded protein level of metabolic syndrome rat model livers, misfolded proteins were gradually increased by severity of symptom. This might indicate folding ability of the cycle was declined and might be affected folding of UGGT.