OBJECTIVE: To study the rapid modeling of KK mouse diet and its effect on related indexes in KK/Upj-Ay/J mice.
Methods: 40 female and male KK/UpjAy/J mice were used for the experiment, and they were divided into 4 groups, which were the common feed group (10 females and 10 males) and the KK mouse feed group (10 females and 10 males). 、Fasting blood glucose group with common diet (10 females and 10 males each), and KK rat diet fasting blood glucose group (10 females and 10 males). Feeding started from 3 weeks until the end of the experiment at 23 weeks. Body weight and fasting blood glucose were measured every week After the experiment, serum was collected to detect biochemical indicators, and pancreas, kidney, and liver were fixed for HE and special staining (insulin immunohistochemical staining for pancreas, PAS staining for liver, and PASM staining for kidney).
Results: KK rat diet could significantly promote the weight gain of KK/Upj-Ay/J mice, increase the fasting blood glucose level of KK/Upj-Ay/J mice, and increase the serum alanine aminotransferase level of KK/Upj-Ay/J mice. (P<0.05). KK rat diet can significantly increase the serum creatinine content of female KK/Upj-Ay/J mice (P<0.05), and significantly increase the serum cholesterol content of male KK/Upj-Ay/J mice (P<0.05). P<0.05), but had no significant effect on the serum cholesterol content of female KK/Upj-Ay/J mice. At the end of the feeding experiment, the pancreas of female KK/Upj-Ay/J mice had obvious pathological changes, but male KK/Upj mice had obvious pathological changes. -Ay/J mice have no obvious effect on the pathological changes of pancreas. It is presumed to be related to the physiological characteristics of male KK/Upj-Ay/J mice. KK mouse diet significantly promotes hepatocyte steatosis in KK/Upj-Ay/J mice. At the end of the feeding experiment, compared with the C57BL/6J group, the renal pathological changes in the common chow-fed group and the KK rat chow-fed group were mainly manifested as tubular protein casts, interstitial nephritis, perivascular inflammation, and glomerular mesangium. Matrix increased. The degree of nephropathy in the KK rat feeding group was more obvious. Compared with the control group, the results of renal PASM staining showed that the glomerular basement membrane of the other two groups did not have dark brown substance deposition, indicating that the glomerular basement membrane was structurally damaged.
CONCLUSION: KK rat diet can promote organ damage in KK/Upj-Ay/J mice, increase fasting blood glucose and body weight, shorten modeling time, and improve modeling uniformity.