Serotonin and Interleukin 10 Can Influence the Blood and Urine Viscosity in Gestational Diabetes Mellitus and Pregnancy-Specific Urinary Incontinence.

Serotonin and interleukin 10 (IL-10) may play a role in gestational diabetes mellitus. Hyperglycemic environment, the detrusor musculature of the bladder and pelvic floor muscles may become damaged, leading to urination problems and urine viscosity in pregnant women with gestational diabetes mellitus and pregnancy-specific urinary incontinence. Urine and blood samples were collected from pregnant women between 24 and 28 weeks of gestation. The serotonin concentration and cytokine IL-10 levels were evaluated in plasma and urine. In the total blood and urine, the viscosity was evaluated in the presence and absence of exogenous serotonin and IL-10. The plasma serotonin levels decreased, while the urine serotonin levels increased in the normoglycemic incontinent (NG-I), hyperglycemic continent (GDM-C), and hyperglycemic incontinent (GDM-I) groups. The IL-10 in the plasma decreased in the GDM-I group and was higher in the urine in the NG-I and GDM-I groups. The blood viscosity was higher, independently of urinary incontinence, in the GDM groups. The serotonin increased the blood viscosity from women with GDM-C and urine in the NG-I, GDM-C, and GDM-I groups. Blood and urine in the presence of IL-10 showed a similar viscosity in all groups studied. Also, no difference was observed in the viscosity in either the blood or urine when in the presence of serotonin and IL-10. These findings suggest that serotonin and IL-10 have the potential to reduce blood viscosity in pregnant women with gestational diabetes and specific urinary incontinence, maintaining values similar to those in normoglycemic women's blood.

Role of dietary food intake patterns, anthropometric measures, and multiple biochemical markers in the development of pregnancy-specific urinary incontinence in gestational diabetes mellitus.

OBJECTIVES: The aim of this study was to assess maternal dietary food intake patterns, anthropometric measures, and multiple biochemical markers in women with gestational diabetes mellitus and pregnancy-specific urinary incontinence and to explore whether antedating gestational diabetes mellitus environment affects the pregnancy-specific urinary incontinence development in a cohort of pregnant women with gestational diabetes mellitus and pregnancy-specific urinary incontinence. METHODS: Maternal dietary information and anthropometric measurements were collected. At 24 wk of gestation, with a fasting venipuncture sample, current blood samples for biochemical markers of hormones, vitamins, and minerals were analyzed. The groups were compared in terms of numerical variables using analysis of variance for independent samples followed by multiple comparisons. RESULTS: Of the 900 pregnant women with complete data, pregnant women in the gestational diabetes mellitus pregnancy-specific urinary incontinence group had higher body mass index during pregnancy, arm circumference, and triceps skinfold than the non-gestational diabetes mellitus continent and non-gestational diabetes mellitus pregnancy-specific urinary incontinence groups, characterizing an obesogenic maternal environment. Regarding dietary food intake, significant increases in aromatic amino acids, branched-chain amino acids, dietary fiber, magnesium, zinc, and water were observed in pregnancy-specific urinary incontinence group compared with the non-gestational diabetes mellitus continent group. Serum vitamin C was reduced in the gestational diabetes mellitus pregnancy-specific urinary incontinence group compared with the non-gestational diabetes mellitus pregnancy-specific urinary incontinence group. CONCLUSIONS: This study emphasizes the necessity for a comprehensive strategy for gestational diabetes mellitus women with pregnancy-specific urinary incontinence in terms of deviation in maternal adaptation trending toward obesity and maternal micronutrients deficiencies.

Disruptive Effect of Organotin on Thyroid Gland Function Might Contribute to Hypothyroidism.

A considerable increase in endocrine abnormalities has been reported over the last few decades worldwide. A growing exposure to endocrine-disrupting chemicals (EDCs) can be one of the causes of endocrine disorders in populations, and these disorders are not only restricted to the metabolic hormone system but can also cause abnormal functions. Thyroid hormone (TH) disruption is defined as an abnormal change in TH production, transport, function, or metabolism, which results in some degree of impairment in body homeostasis. Many EDCs, including organotin compounds (OTCs), are environmental contaminants that are commonly found in antifouling paints used on ships and in several other industrial procedures. OTCs are obesogenic and can disrupt TH metabolism; however, abnormalities in thyroid function resulting from OTC exposure are less well understood. OTCs, one of the most prevalent EDCs that are encountered on a daily basis, modulate the thyroid axis. In most toxicology studies, it has been reported that OTCs might contribute to hypothyroidism.