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Selenoproteins and renal programming in metabolic syndrome-exposed rat offspring
María Luisa Ojeda1, Fátima Nogales, Alejandra Serrano
1Department of Physiology, Faculty of Pharmacy, Seville University, 41012 Seville, Spain. fnogales@us.es.
Insights
Maternal metabolic syndrome in rats impairs kidney function and elevates blood pressure in pups. Increased selenium and selenoproteins in MS pups may offer some protection against oxidative stress.
Area of Science:
- Perinatal programming
- Renal physiology
- Nutritional biochemistry
Background:
- Maternal metabolic syndrome (MS) impacts offspring cardiometabolic health, particularly selenium (Se) status and selenoprotein expression.
- Kidney programming and antioxidant selenoprotein status in MS offspring remain understudied.
Purpose of the Study:
- To investigate kidney programming, antioxidant selenoprotein status, and related molecular pathways in offspring exposed to maternal MS.
- To evaluate the functional and hypertensive consequences of MS exposure in pups.
Main Methods:
- Two groups of dam rats: Control (0.1 ppm Se) and MS (65% fructose, 0.1 ppm Se).
- Assessment of kidney Se, selenoprotein (GPx1, GPx3, GPx4, SelP) expression, oxidative balance, AMPK, and NF-κB.
- Evaluation of kidney function (albuminuria, creatinine clearance), electrolytes, and systolic blood pressure.
Main Results:
- MS pups exhibited increased kidney lipid peroxidation, Se, selenoproteins, and NF-κB, with decreased AMPK activation.
- MS pups showed albuminuria, low creatinine clearance, hypernatremia, hyperaldosteronemia, and hypertension.
- Elevated Se and selenoproteins in MS pups appeared to mitigate higher lipid oxidation.
Conclusions:
- Maternal MS induces significant renal impairment, oxidative stress, and hypertension in offspring.
- While increased Se and selenoproteins show some protective effects against renal oxidative damage, further research is needed to clarify their global role in MS-induced kidney programming.
Abstract:
Maternal metabolic syndrome (MS) during gestation and lactation leads to several cardiometabolic changes related to selenium (Se) status and selenoprotein expression in offspring. However, little is known about kidney programming and antioxidant selenoprotein status in MS pups. To gain more knowledge on this subject, two experimental groups of dam rats were used: Control (Se: 0.1 ppm) and MS (fructose 65% and Se: 0.1 ppm). At the end of lactation, Se deposits in kidneys, selenoprotein expression (GPx1, GPx3, GPx4 and selenoprotein P), oxidative balance and AMP-activated protein kinase (AMPK) and activated transcriptional factor NF-κB expression were measured. Kidney functional parameters, albuminuria, creatinine clearance, aldosteronemia, and water and electrolyte balance, were also evaluated. One week later systolic blood pressure was measured. Lipid peroxidation takes place in the kidneys of MS pups and Se, selenoproteins and NF-κB expression increased, while AMPK activation decreased. MS pups have albuminuria and low creatinine clearance which implies glomerular renal impairment with protein loss. They also present hypernatremia and hyperaldosteronemia, together with a high renal Na+ reabsorption, leading to a hypertensive status, which was detected in these animals one week later. Since these alterations seem to be related, at least in part, to oxidative stress, the increase in Se and selenoproteins found in the kidneys of these pups seems to be beneficial, avoiding a higher lipid oxidation. However, in order to analyze the possible global beneficial role of Se in kidneys during MS exposure, more data are necessary to document the relationships between GPx4 and NF-κB, and SelP and AMPK in kidneys.
