Increased food intake, reduced physical activity, and alteredmetabolic processes are the variables affecting energy balanceinducing obesity. Obesity, in association with diabetes and hyper-tension, can contribute to the increased incidence of chronic kid-ney diseases (CKD). On the other hand, kidney has an importantrole in the complex inter-organ communication occurring withthe development of inflammation and fibrosis during obesity.Down-regulation of the dopamine D2 receptor results inincreased renal expression of injury markers and proinflammato-ry factors independent from blood pressure increase. In obeseZucker rats, defective D1-like and D2-like receptors expression isnot inherited but contributes to hyperinsulinemia associated withobesity. This study was done to clarify in rats with Diet-InducedObesity (DIO) the possible relationships between high-fat diet,kidney damage and possible inflammatory processes.Histochemical and immunohistochemical techniques were used.Rats of 7 weeks of age exposed to high-fat diet were used. After5 weeks, when rat body weight was increased significantly com-pared to the control group (CHOW), were designated as DIOrats. Rats were followed for other 12 weeks. After 17 weeks ofa high-fat diet, systolic blood pressure, glycaemia and insulin lev-els were higher in DIO rats compared to CHOW. The kidney ofDIO rats showed glomeruli partially collapsed with increasedthickness of the glomerular basement membrane. Analysis forIL-1brevealed in DIO rats an increased expression at the levelof glomeruli and in basal portion of proximal and convolutedtubules cells. Changes in the expression of the D1-like receptors,in particular of the D5 receptor, and D2-like dopamine receptorswas evident in the DIO rats, compared to control animals. Thesefindings indicate that in DIO rats, nephropathy is a complex phe-nomenon, and could be related to inflammation induced by bodyweight gain or related risk factors such as hypertension and/orhyperglycemia.
Kidney changes in obese rats: evidence for nephropathy related to diet
Traini E;Martinelli I;Tomassoni D;Moruzzi M;Gabrielli MG;Micioni Di Bonaventura MV;Cifani C;Tayebati SK;Amenta F.
2019-01-01
Abstract
Increased food intake, reduced physical activity, and alteredmetabolic processes are the variables affecting energy balanceinducing obesity. Obesity, in association with diabetes and hyper-tension, can contribute to the increased incidence of chronic kid-ney diseases (CKD). On the other hand, kidney has an importantrole in the complex inter-organ communication occurring withthe development of inflammation and fibrosis during obesity.Down-regulation of the dopamine D2 receptor results inincreased renal expression of injury markers and proinflammato-ry factors independent from blood pressure increase. In obeseZucker rats, defective D1-like and D2-like receptors expression isnot inherited but contributes to hyperinsulinemia associated withobesity. This study was done to clarify in rats with Diet-InducedObesity (DIO) the possible relationships between high-fat diet,kidney damage and possible inflammatory processes.Histochemical and immunohistochemical techniques were used.Rats of 7 weeks of age exposed to high-fat diet were used. After5 weeks, when rat body weight was increased significantly com-pared to the control group (CHOW), were designated as DIOrats. Rats were followed for other 12 weeks. After 17 weeks ofa high-fat diet, systolic blood pressure, glycaemia and insulin lev-els were higher in DIO rats compared to CHOW. The kidney ofDIO rats showed glomeruli partially collapsed with increasedthickness of the glomerular basement membrane. Analysis forIL-1brevealed in DIO rats an increased expression at the levelof glomeruli and in basal portion of proximal and convolutedtubules cells. Changes in the expression of the D1-like receptors,in particular of the D5 receptor, and D2-like dopamine receptorswas evident in the DIO rats, compared to control animals. Thesefindings indicate that in DIO rats, nephropathy is a complex phe-nomenon, and could be related to inflammation induced by bodyweight gain or related risk factors such as hypertension and/orhyperglycemia.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
