Selenium supplementation during pregnancy and lactation promotes metabolic changes in Wistar rats' offspring

Abstract

Epidemiological and animal studies have demonstrated a strong association between selenium (Se) supplementation and metabolic disorders, we aimed to evaluate whether maternal Se supplementation was able to change metabolic parameters in rats' offspring. Moreover, as Se is a deiodinase (DIO) cofactor, we decided to investigate how thyroid hormones (THs) would be involved in such metabolic changes.Thereby, two groups (n = 6, ~250 g) of female Wistar rats underwent isotonic saline or sodium selenite (1 mg/kg, p.o.) treatments. Although there were no significant differences in body weight between groups, the Se treatment during pregnancy and lactation increased milk intake and the visceral white adipose tissue (WAT) in offspring.The rats whose mothers were treated with Se also presented an improvement in the glucose tolerance test and in the glucose-stimulated insulin secretion. Regarding the lipid metabolism, the Se group had a reduction of triglycerides in the liver and in WAT.These metabolic changes were accompanied by an increase in serum triiodothyronine (T 3 ) and in DIO 2 expression in brown adipose tissue (BAT). We further demonstrate an increased expression of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) and nuclear respiratory factor-1 (NRF-1) mRNA in the liver. In adulthood offspring, Se supplementation programs thyroid function, glucose homeostasis, and feeding behaviour. Taken together, there is no indication that Se programming causes insulin resistance. Moreover, we conjecture that these metabolic responses are induced by increased thyroxine (T 4 ) to T 3 conversion by DIO2 in BAT and mediated by altered transcription factors expression associated with oxidative metabolism control in the liver. K E Y W O R D Sdeiodinase type II, metabolism, offspring, selenium supplementation, thyroid hormone | 1273 LAUREANO-MELO Et AL.

The association between serum selenium level and gestational diabetes mellitus: A systematic review and meta‐analysis

“…Selenoproteins related to oxidative stress, such as glutathione peroxidase, thioredoxin reductase and deiodinase, seem to be important for the changes in GDM 22 . With the increasing incidence rate of GDM, an increasing number of studies have been conducted on animal models, and the physiological and pathological mechanisms of GDM have been evaluated in humans 23–25 . Exploration of the relationship between GDM and serum selenium level and its possible mechanism can provide solutions to reduce the incidence rate of GDM in the future.…”

“…22 With the increasing incidence rate of GDM, an increasing number of studies have been conducted on animal models, and the physiological and pathological mechanisms of GDM have been evaluated in humans. [23][24][25] Exploration of the relationship between GDM and serum selenium level and its possible mechanism can provide solutions to reduce the incidence rate of GDM in the future. Although there has been a previous metaanalysis 26 with several of studies on the effects of micronutrients on GDM, we still believe that restart of this analysis is warranted.…”

The Role of Selenoprotein Tissue Homeostasis in MetS Programming: Energy Balance and Cardiometabolic Implications

“…These authors concluded that cardiovascular alterations took place when IUGR appear and that they are probably related to the impaired thyroid dysfunction that Se deficiency offspring present by decreasing the activity of the selenoproteins DIOs [ 120 , 121 ]. Laureano-Melo et al observed that maternal Se supplementation to Wistar rats was able to program carbohydrate and lipid metabolism, endocrine homeostasis, and feeding behavior, even in the adult offspring [ 122 ]. They suggested that metabolic effects were induced by THs disbalance together with the antioxidant mechanisms.…”

The Effect and Potential Mechanism of Maternal Micronutrient Intake on Offspring Glucose Metabolism: An Emerging Field

“…Adequate ingestion of Se is basic nutrition, as its deficiency results in pregnancyrelated complications, metabolic disorders, and other disorders in offspring (108,109). Melo et al found that in rats, maternal Se increases insulin secretion and glucose tolerance at 80 days of age (110). However, Zeng et al found that excessive Se in the mother's diet led to insulin resistance in offspring at 112 days of age (111).…”