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(TSH) has a vital importance for regulating thyroid hormone release along with
growth of thyroid gland, secreted from anterior pituitary. It stimulates thyroid follicular cells to release T3 (20%), T4 (80%) and thyroxine [37].
Evidence has also suggested altered thyroid hormone levels upon paraben exposure during pregnancy [38]. The balance of thyroid hormone during pregnancy is
essential because fetus depends on maternal thyroid hormones, required for fetal
brain differentiation and neuronal development. So, deficiency of this hormone can
lead to neurodevelopmental problems [39–41]. So, cosmetic products (major source
of paraben exposure) should be principally avoided during pregnancy.
In addition to this, hyperthyroidism along with hypothyroidism give rise to insulin resistance, a potential hallmark of metabolic syndromes. Additionally, altered
thyroid hormones are also associated with diabetes mellitus, dislipoproteinemia,
arterial hypertension, and changes in body weight [42]. Although results of paraben
exposure and disturbance in thyroid hormone levels are more prominent in animal
studies, further human studies associating parabens and thyroid hormone levels are
required to confirm potential findings of animal studies [36].
Influence of Parabens on Testosterone
Testosterone is a primary hormone essential for the developmental growth and participates pivotal role in maintaining male phenotype throughout the life. Unlike to
women, where estrogen level decline suddenly during menopause, testosterone
level in men decreases gradually with aging [43]. Exposure of parabens is interlinked with diminished testosterone in experimental studies on rats, also adversely
affects male reproductive functions. Propyl treated rats also demonstrated significant decrease in daily sperm production [44]. Likewise, paraben’s exposure has
illustrated undesirable effects in animals, yet human epidemiologic studies are lacking. Although one epidemiologic study presented no relationship between hormonal
level and urinary parabens, yet modest sample size and intraindividual variability in
exposure have limited to confirm any suitable results [45].
Biochemical evidences demonstrate the involvement of testosterone in enhancing glucose utilization by promoting glucose uptake, mitochondrial oxidative phosphorylation and glycolysis. Additionally, testosterone also mediates role in lipid
homeostasis in insulin responsive target tissues like skeletal muscles, liver, and adipose tissues [46]. Accordingly, testosterone also possesses defensive action on pancreatic β-cells [47]. Ultimately, low testosterone level accelerates the risks for
insulin resistance and evidently give rise to diabetes. Also, low level of testosterone
is observed in insulin resistant patients [48, 49]. Consequently, low testosterone
levels (either due to paraben exposure or other reason) are interlinked with raised
insulin resistance, impaired mitochondrial function, increased triglyceride levels,
diminished HDL cholesterol and also give rise to five-times increase in risks for
cardiovascular diseases [50–52].
K. Haider et al.
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