Background: Menopause, a natural step in woman`s life aging process, is associated with increased risk of metabolic diseases. Salt, is an essential micronutrient, commonly added to food. However, studies addressing the metabolic effects of high salt intake are controversial and limited.
Objective: The present study was designed to determine the changes imposed by increased salt consumption on glucose and lipid homeostasis in ovariectomized rats that mimics the estrogen-deprived condition in postmenopausal women.
Material and Methods: Thirty six adult female albino Wister rats were allocated into 3 equal groups: Control group, ovariectomized group, and high salt ovariectomized group which received high salt (2%NaCl) solution for 2 months. Rats were subjected to estimation of body weight (BW), body mass index (BMI), waist circumference (WC), and visceral fat weight. Glucose uptake by diaphragm and glucose output by kidneys were determined. Also, levels of glucose, lipid profile, malondialdehyde, catalase, insulin, estradiol and tumor necrosis factor-α were measured. Pancreatic and hepatic tissues were examined histopathologically. Also, caspase-3 was assessed in pancreas by immunohistochemistry.
Results: High salt ovariectomized group showed significant decrease in final WC, and significant increase in serum insulin, HOMA-IR, serum levels of MDA and TNF-α compared to the ovariectomized group. There were significant increases in plasma levels of glucose, triglycerides, total cholesterol, LDL-C, catalase, and AI, and significant decrease in glucose uptake by diaphragm, and plasma HDL-C in high salt group compared to control group.
     As compared to ovariectomized group, the pancreas in salt loaded group showed decreased number of islets of Langerhans and fatty degeneration together with increased caspase-3. Liver histology was also worsened, and hepatocytes showed ballooning, steatosis and inflammatory infiltration together with massive amounts of collagen fibers around portal tract. 
Conclusion: High salt intake exacerbated the hyperglycemia and insulin resistance, intensified pancreatic apoptosis and hepatic fatty, and degenerative changes. These effects could be explained by salt loading-induced exacerbation and exaggeration of oxidative and inflammatory influences of ovariectomy.