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Objective: To investigate the association between gestational blood lipids and thyroid stimulating hormone (TSH) levels and pregnancy outcomes of patients with subclinical hypothyroidism (SCH). Methods: In this retrospective observational study, we analyzed the clinical data of 82 patients (case group) with gestational SCH treated in our hospital from January 2021 to January 2022 at gestational weeks 25-33 and grouped them according to whether SCH was well controlled by treatment (case Group-A: well controlled, n=55; case Group-B: poorly controlled, n=27), and the clinical data of 41 pregnant women (control group) undergoing physical examination during the same period. After comparing the blood lipids and TSH levels of the three groups, we compared their adverse pregnancy outcomes to assess the possible correlations between blood lipids and TSH levels and pregnancy outcomes. Results: The levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and TSH in the case Group-B were significantly higher than those in the case Group-A and the control group (P<0.05). Compared with case Group-B and the control group, the incidence of premature delivery, abortion and neonatal growth restriction was higher in case Group-A (P<0.05). Among 82 patients in the case group 42 presented adverse pregnancy outcomes. The levels of TC, TG, LDL-C and TSH in mothers and infants in the adverse outcome group were significantly higher than those in the favorable outcome group (P<0.05). Our Pearson analysis results showed that the levels of TC, TG and LDL-C were positively correlated with the TSH levels and the pregnancy outcomes, and that TSH was positively correlated with pregnancy outcomes (P<0.05). Conclusion: The levels of TC, TG, LDL-C and TSH in patients with poorly controlled SCH were increased during pregnancy, and were associated with the pregnancy outcomes and positively correlated with each other. [ABSTRACT FROM AUTHOR]

The intestinal microbiota regulates mammalian lipid absorption, metabolism, and storage. We report that the microbiota reprograms intestinal lipid metabolism in mice by repressing the expression of long noncoding RNA (lncRNA) Snhg9 (small nucleolar RNA host gene 9) in small intestinal epithelial cells. Snhg9 suppressed the activity of peroxisome proliferator–activated receptor γ (PPARγ)—a central regulator of lipid metabolism—by dissociating the PPARγ inhibitor sirtuin 1 from cell cycle and apoptosis protein 2 (CCAR2). Forced expression of Snhg9 in the intestinal epithelium of conventional mice impaired lipid absorption, reduced body fat, and protected against diet-induced obesity. The microbiota repressed Snhg9 expression through an immune relay encompassing myeloid cells and group 3 innate lymphoid cells. Our findings thus identify an unanticipated role for a lncRNA in microbial control of host metabolism. [ABSTRACT FROM AUTHOR]