Pancreas metabonomic profiles of the type 2 diabetic rats' induced by streptozotocin(STZ) and high-sugar, high fat diet on the treatment of Renshenjian decoction(RSJD) after 8 weeks were investigated.In this study, 48 Rats were randomly divided into four groups: normal control (NC), Pathological model (PM), Renshenjian decoction(RSJD 3.76 g·kg⁻¹) and glimepiride control (GC 0.04 mg·kg⁻¹). They are induced insulin resistance model of type 2 diabetes mellitus by streptozotocin(STZ) after 4 weeks' high-sugar, high fat diet except for NC. After sucessful modeling, they are given intragastric administration respectively with same amount of saline, RSJD and glimepiride in 4 weeks. At the end of the 8th week, the pancreatic tissue of rats in each group was collected, and the ¹H-NMR spectrum was collected after being treated by certain method, and analyzed by principal component analysis (PCA). Compared with NC's rats, we found PM's a significant elevation in the level of leucine/isoleucine, valine, lactic acid, creatine but reduction in the level of inose and less obvious changes in the level of creatine, cholic acid, taurine in pancreatic extract. After having been recieved RSJD, reduction level in leucine/isoleucine, valine, alanine, creatine, choline, taurine are also found in pancreatic extract of RSJD's rats, together with the increase of creatinine and tryptophan levels. The results showed that RSJD could regulate the level of amino acids in pancreas of IR rats, promoting a recovery in the process of metabolism. It's helpful to simulate the metabolic changes of IR rats via ¹H-NMR for a further understanding to study the mechanism how RSJD treat IR rats.

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and challenging entity which can be life threatening and is associated with many medications. Yet, Glimepiride has never been reported as offending agent. We present here the first case of Glimepiride induced DRESS syndrome. A 40-year-old male with type 2 diabetes mellitus was prescribed Glimepiride. One month later, the patient presented with diffuse rash, fever, swelling of extremities and jaundice. The leucocyte count at presentation was 22,000 cells/microL and absolute eosinophil count 5,400 cells/microL, with no atypical cells on peripheral blood smear. Skin biopsy was non-specific. Other sources of infections such as parasitic infections, HIV, viral hepatitis were ruled out. Patient improved symptomatically on discontinuation of Glimepiride and improved dramatically on steroids. DRESS syndrome as a possible complication of Glimepiride should be considered by clinicians. According to RegiSCAR, our case was categorized as definitive with score of 7. In the vast majority of reported cases, they are classified as probable cases.

The therapeutic use of glimepiride and gliclazide shows substantial inter-individual variation in pharmacokinetics and pharmacodynamics in human populations, which might be caused by genetic differences among individuals. The aim of this study was to assess the effect of CYP2C9 and OATP1B1 genetic polymorphisms on the metabolism and transport of glimepiride and gliclazide. The uptake of glimepiride and gliclazide was measured in OATP1B1*1a, *5 and *15-HEK293T cells, and their metabolism was measured using CYP2C9*1, *2 and *3 recombinase by LC-MS. Glimepiride in OATP1B1*1a, *5 and *15-HEK293T cells had Vmax values of 155 ± 18.7, 80 ± 9.6, and 84.5 ± 8.2 pmol/min/mg, while gliclazide had Vmax values of 15.7 ± 4.6, 7.2 ± 2.5, and 8.7 ± 2.4 pmol/min/mg, respectively. The clearance of glimepiride and gliclazide in OATP1B1*5 and *15 was significantly reduced compared to the wild-type. Glimepiride in the presence of CYP2C9*1, *2 and *3 recombinase had Vmax values of 21.58 ± 7.78, 15.69 ± 5.59, and 9.17 ± 3.03 nmol/min/mg protein, while gliclazide had Vmax values of 15.73 ± 3.11, 10.53 ± 4.06, and 6.21 ± 2.94 nmol/min/mg protein, respectively. The clearance of glimepiride and gliclazide in CYP2C9*2 and *3 was significantly reduced compared to the wild-type. These findings collectively indicate that OATP1B1*5 and *15 and CYP2C9*2 and *3 have a significant effect on the transport and metabolism of glimepiride and gliclazide.

This class of medications represents a group of anti-hyperglycemic agents mainly used in the treatment of type 2 diabetes mellitus. Sulfonylureas, commonly divided into first and second generations, can be utilized as adjuvant therapy with metformin in patients not at target hemoglobin A1c after 3 months on biguanides. If a patient’s hemoglobin A1c initially is greater than 9.0%, providers can consider combination therapy with metformin and a sulfonylurea or other anti-hyperglycemic agent. Additionally, sulfonylurea monotherapy can be considered in patients intolerant to metformin or in those who have a contraindication to this medication. Sulfonylureas can be used in combination with any other class of oral diabetic medications besides meglitinides. Infants with permanent neonatal diabetes also tend to respond well to sulfonylurea treatment. Examples of first-generation sulfonylureas include chlorpropamide, tolazamide, and tolbutamide, while second-generation sulfonylureas include glipizide, gliclazide, and glyburide. Glimepiride occasionally is referred to as a third-generation medication, though it commonly is classified as second-generation. Furthermore, chlorpropamide, glyburide, and glimepiride have a prolonged duration of action when compared to short-acting medications such as gliclazide and tolbutamide. Due to their low cost, wide availability, and effectiveness, sulfonylureas have remained a frequently prescribed medication despite potential hypoglycemic risks.

Because no information is available on the use of glimepiride during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant. Monitoring of the breastfed infant's blood glucose is advisable during maternal therapy with hypoglycemic agents.[1][2]