BackgroundThis study aimed to investigate the relationships among overactive bladder (OAB) symptom severity, bother, help-seeking behavior, and quality of life (QOL) in patients with type 2 diabetes.MethodsA total of 127 diabetic patients, aged at least 18 years, with overactive bladder from a hospital in Shandong Province, China, were recruited for this study. Symptom severity, bother, and quality of life were assessed using the Overactive Bladder Symptom Score (OABSS), Patient Perception of Bladder Condition (PPBC), and Overactive Bladder Questionnaire Short Form (OAB-q SF), respectively. Help-seeking behavior was assessed by asking patients whether they consulted health care professionals or received treatment for their bladder problems. A two-step path analysis was performed to analyze the data.ResultsOAB symptom severity was directly associated with lower levels of QOL, and the strength of this association was no longer significant when taking bother and help-seeking behavior into account. Bother increased with OAB symptom severity, and patients with bothersome OAB tended to have lower levels of QOL. Moreover, bother increased help-seeking behavior; however, patients who sought help tended to have lower levels of QOL.ConclusionsOur findings highlight the role of bother and help-seeking behavior in the relationship between OAB symptom severity and QOL. To improve a patient’s QOL, health care providers should focus not only on symptom bother but also on dysfunctional help-seeking patterns.

Menopause is associated with dyslipidemia and an increased risk of cardio-cerebrovascular disease. The classic view assumes that the underlying mechanism of dyslipidemia is attributed to an insufficiency of estrogen. In addition to a decrease in estrogen, circulating follicle-stimulating hormone (FSH) levels become elevated at menopause. In this study, we find that blocking FSH reduces serum cholesterol via inhibiting hepatic cholesterol biosynthesis. First, epidemiological results show that the serum FSH levels are positively correlated with the serum total cholesterol levels, even after adjustment by considering the effects of serum estrogen. In addition, the prevalence of hypercholesterolemia is significantly higher in peri-menopausal women than that in premenopausal women. Furthermore, we generated a mouse model of FSH elevation by intraperitoneally injecting exogenous FSH into ovariectomized (OVX) mice, in which a normal level of estrogen (E2) was maintained by exogenous supplementation. Consistently, the results indicate that FSH, independent of estrogen, increases the serum cholesterol level in this mouse model. Moreover, blocking FSH signaling by anti-FSHβ antibody or ablating the FSH receptor (FSHR) gene could effectively prevent hypercholesterolemia induced by FSH injection or high-cholesterol diet feeding. Mechanistically, FSH, via binding to hepatic FSHRs, activates the Gi2α/β-arrestin-2/Akt pathway and subsequently inhibits the binding of FoxO1 with the SREBP-2 promoter, thus preventing FoxO1 from repressing SREBP-2 gene transcription. This effect, in turn, results in the upregulation of SREBP-2, which drives HMGCR nascent transcription and de novo cholesterol biosynthesis, leading to the increase of cholesterol accumulation. This study uncovers that blocking FSH signaling might be a new strategy for treating hypercholesterolemia during menopause, particularly for women in peri-menopause characterized by FSH elevation only.

Aim: Excess dietary fat intake can induce lipotoxicity in non-adipose tissues. The aim of this study was to observe the effects of dietary high-fat lard intake on thyroid in rats. Methods: Male Sprague-Dawley rats were fed a high-fat lard diet for 24 weeks, and then the rats were fed a normal control diet (acute dietary modification) or the high-fat lard diet for another 6 weeks. The serum lipid profile, total thyroxine (TT4), free thyroxine (FT4) and thyrotropin (TSH) levels were determined at the 12, 18, 24 and 30 weeks. High-frequency ultrasound scanning of the thyroid glands was performed at the 24 or 30 weeks. After the rats were sacrificed, the thyroid glands were collected for histological and immunohistochemical analyses. Results: The high-fat lard diet significantly increased triglyceride levels in both the serum and thyroid, and decreased serum TT4 and FT4 levels in parallel with elevated serum TSH levels. Ultrasonic imaging revealed enlarged thyroid glands with lowered echotexture and relatively heterogeneous features in the high-fat lard fed rats. The thyroid glands from the high-fat lard fed rats exhibited enlarged follicle cavities and flattened follicular epithelial cells under light microscopy, and dilated endoplasmic reticulum cisternae, twisted nuclei, fewer microvilli and secretory vesicles under transmission electron microscopy. Furthermore, the thyroid glands from the highfat lard fed rats showed markedly low levels of thyroid hormone synthesis-related proteins TTF-1 and NIS. Acute dietary modification by withdrawal of the high-fat lard diet for 6 weeks failed to ameliorate the high-fat lard diet-induced thyroid changes. Conclusion: Dietary high-fat lard intake induces significant thyroid dysfunction and abnormal morphology in rats, which can not be corrected by short-term dietary modification.

Objectives. To evaluate the effect of levothyroxine (LT4) replacement therapy on nonalcoholic fatty liver disease (NAFLD) in subclinical hypothyroidism (SCH) patients. Methods. This study was a post hoc analysis of a randomized controlled trial and involved 33 significant and 330 mild SCH patients. All of the significant SCH patients received LT4 supplement. The mild SCH patients were grouped as LT4 treated or not. After 15 months of follow-up, prevalence of NAFLD in each group was reevaluated. Subgroup analysis was conducted in mild SCH patients with dyslipidemia. Results. After treatment with LT4, the prevalence of NAFLD in significant SCH patients reduced from 48.5% to 24.2% (p = 0.041). In mild SCH patients, prevalence of NAFLD and serum alanine aminotransferase (ALT) was not significantly affected by LT4 supplementation. Nonetheless, mild SCH patients with dyslipidemia who received LT4 treatment experienced decreases in the prevalence of NAFLD and serum ALT levels (p < 0.05 for both). In contrast, these parameters remained comparably stable in patients who were not treated. Conclusion. LT4 supplementation has benefits on NAFLD in significant SCH patients or mild SCH patients with dyslipidemia. For NAFLD patients with SCH, appropriate supplementation of LT4 may be an effective means of controlling NAFLD. The original trial was registered with ClinicalTrials.gov (NCT01848171).

Our findings suggested that hypertriglyceridemia was positively associated with the risk for SCH.

Objective: To evaluate the relationship between serum total testosterone (TT) level and lipid profile after adjusting for some traditional confounding factors, free thyroid hormones and TSH in Chinese men. Methods: This was a retrospective study based on an epidemiological investigation including 11 000 subjects. Bivariate and partial correlation analysis, multiple linear regression analysis, and a general linear model were used to assess the influence of TT on the lipid profile. Additionally, the odds ratios (ORs) (95% CIs) for hypertriglyceridemia and low HDL-C in relation to TT categories were calculated using logistic regression analysis. Results: A total of 4114 subjects whose mean age was 56.04G8.75 years were finally analyzed. There was a significant linear trend toward lower total cholesterol (TC), lower triglycerides (TG), and higher HDL-C with increasing serum TT, which remained significant after adjusting for age, BMI, fasting blood glucose, systolic blood pressure, free triiodothyronine, free thyroxine, and TSH. Compared with the bottom quartile of TT, the adjusted OR (95% CI) for hypertriglyceridemia and low HDL-C was 0.082 (0.048-0.138, PZ0.000) and 0.669 (0.503-0.891, PZ0.006) respectively in the top quartile of TT. Conclusions: TT was correlated negatively and linearly with TC, TG, and LDL-C and positively and linearly with HDL-C. Low TT might have adverse effects on the lipid profile and thus represent a risk factor for hypercholesterolemia, hypertriglyceridemia, high LDL-C, and low HDL-C, suggesting the importance of maintaining an appropriate TT level in men.

Striatal circuit dysfunction is implicated in smoking behaviors and lapses during abstinence attempts. However, little is known about whether the structural connectivity of striatal tracts can be used to predict abstinence-induced craving and lapses. The tract strengths of striatal circuits were compared in 53 male nicotine-dependent cigarette smokers and 58 matched nonsmokers, using seed-based classification by diffusion tensor imaging (DTI) probabilistic tractography with 10 a priori target masks. A 12-h abstinence procedure was then employed, after which 31 individuals abstained and 22 lapsed. Linear regression and binary logistic regression was conducted to test whether the tract strength of frontostriatal circuits was associated with craving changes in abstainers and predicted lapse in smokers. Compared with nonsmokers, in the left hemisphere, smokers showed weaker tract strength in striatum-medial orbitofrontal cortex (mOFC), striatum-ventral lateral prefrontal cortex (vlPFC), striatum-inferior frontal gyrus (IFG) and striatum-posterior cingulate cortex (PCC) (Bonferroni corrected, p < 0.05/20 = 0.0025). In abstainers, the abstinence-induced increases in craving were associated with the tract strength of the left striatum-mOFC and striatum-vlPFC. The tract strength of left striatum-dorsolateral PFC (dlPFC) predicted lapse in smokers with an accuracy of 68.3%. These results provide system-level insights into the weaker tract strength of frontostriatal circuits in male smokers and their potential roles as neuroimaging markers for abstinence-induced craving and risk of lapse. Future studies in female smokers are needed to determine if this generalizes across genders.

Primary insomnia (PI) is associated with deteriorating attention, memory, physical and mood complaints. Based on the extensive literature demonstrating the critical roles of the thalamus in sleep regulation, we hypothesized that insomnia would be associated with functional and structural changes of the thalamus. This information is needed to better understand the neural mechanisms of insomnia, and would be useful for informing future attempts to alleviate or treat insomnia symptoms. Twenty-seven PI patients and 39 matched healthy controls were included in the present study. Subcortical volume and resting state functional connectivity (RSFC) of thalamus were compared between groups, and the relationships between neuroimaging differences and clinical features, including the Pittsburgh Sleep Quality Index (PSQI), the Insomnia Severity Index Scale (ISI), the Self-Rating Anxiety Scale (SAS) and the Self-Rating Depression Scale (SDS), also be explored. Compared with the control group, the PI group showed significantly reduced volume of thalamus. In addition, several brain regions showed reduced RSFC with thalamus in PI patients, such as anterior cingulate cortex (ACC), orbitofrontal cortex, hippocampus, caudate and putamen. Correlation analyses revealed that, several of these RSFC patterns were negatively correlated with PSQI score among PI patients, including thalamic connections with the putamen, caudate, hippocampus. Negative correlation was also observed between the RSFC strength of right thalamus-right ACC and SDS score in PI patients. This work demonstrates the structural and functional abnormalities of the thalamus in PI patients that were associated with key clinical features of insomnia. These data further highlight the important role of the thalamus in sleep and PI.