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Obesity and metabolic syndrome induce hyperfiltration, glomerulomegaly, and albuminuria in obese ovariectomized female mice and obese male mice. 2021
Obese patients with metabolic syndrome have a high risk of chronic kidney disease. The prevalence of obesity, metabolic syndrome, and insulin resistance increase in women after menopause, as does the risk of chronic kidney disease. This may indicate an interaction between obesity, metabolic syndrome, and menopause in the induction of renal damage. However, the pathogenesis of kidney disease in postmenopausal obese women is poorly understood. We investigated the interaction of an obesogenic diet and menopause on renal dysfunction in ovariectomized and non-ovariectomized lean (n = 8 and 17) and obese (n = 12 and 20) female mice. Obese (n = 12) and lean (n = 10) male mice were also studied. Glucose metabolism, insulin resistance, and kidney function were evaluated with gold standards procedures. Changes in kidney histology and lipid deposition were analyzed. Females had a lower number of glomeruli than males at baseline. Only female ovariectomized obese animals developed insulin resistance, hyperglycemia, and kidney damage, evidenced as glomerulomegaly, glomerular hyperfiltration, and increased urinary albumin excretion, despite a similar increase in weight than obese non-ovariectomized female mice. Male obese mice developed hyperglycemia, insulin resistance, and hyperfiltration without major renal histological changes. Males on high fat diet showed higher renal lipid content and females on high fat diet (ovariectomized or non-ovariectomized) showed higher total cholesterol content than males. In mice, there is a clear interplay between obesity, metabolic syndrome, and menopause in the induction of kidney damage.
