TSH-stimulated hepatocyte exosomes modulate liver-adipose triglyceride accumulation via the TGF-β1/ATGL axis in mice.

Subclinical hypothyroidism (SCH) contributes to obesity, with the liver acting as a crucial metabolic regulator. Thyroid-stimulating hormone (TSH) affects systemic lipid balance, potentially linking SCH to obesity. While the direct impact of TSH on hepatic lipid metabolism has been extensively documented, its role in modulating lipid dynamics in peripheral organs through liver-mediated pathways remains insufficiently understood.

Exploring the link between obesity and hypothyroidism in autoimmune thyroid diseases: a metabolic perspective.

The management of primary hypothyroidism demands a comprehensive approach that encompasses both the implications of autoimmune thyroid disease and the distinct effects posed by obesity and metabolic irregularities. Despite its clinical importance, the interplay between obesity and hypothyroidism, especially in the context of metabolic perspectives, is insufficiently explored in existing research. This study endeavors to classify hypothyroidism by considering the presence of autoimmune thyroid disease and to examine its correlation with various metabolic obesity phenotypes.

Expression of apelin‑13 and its negative correlation with TGF‑β1 in patients with diabetic kidney disease.

Diabetic kidney disease (DKD) is a severe microvascular complication of diabetes, one key feature of which includes renal fibrosis. As apelin is an adipokine closely related to diabetes, the present study aimed to evaluate apelin-13 expression levels and the relationship between apelin-13 and disease indicators in patients with diabetic kidney disease (DKD). The present case-control study enrolled 70 patients with diabetes, including 31 with diabetic kidney disease (DKD group), 39 without DKD (non-DKD group) and 30 healthy controls.

The effect of hyperthyroidism on cognitive function, neuroinflammation, and necroptosis in APP/PS1 mice.

Background: Increasing evidence has linked the thyroid dysfunction to the pathogenesis of dementia. Evidence from clinical studies has demonstrated that hypothyroidism is related to an increased risk of dementia. But the association of hyperthyroidism with dementia is largely unknown.

Association of Obesity based on Different Metabolic Status with Risk of Gout Occurrence in Patients: A National Study.

Background: Obesity often co-exists with metabolic abnormalities, but the results of studies on the relationship between obesity, metabolic abnormalities and the risk of gout are inconsistent.

Objectives: We aimed to study whether there was a mutual regulation between obesity, metabolic abnormalities and the risk of gout.

Methods: We conducted a cross-sectional study to expound the association between obesity based on different metabolic statuses and the risk of gout.

The effect of on insulin sensitivity: A proteomic analysis in a -overexpressed high-fat diet mouse model.

Background: Previous research has shown a tight relationship between the G0/G1 switch gene 2 (G0S2) and metabolic diseases such as non-alcoholic fatty liver disease (NAFLD) and obesity and diabetes, and insulin resistance has been shown as the major risk factor for both NAFLD and T2DM. However, the mechanisms underlying the relationship between G0S2 and insulin resistance remain incompletely understood. Our study aimed to confirm the effect of G0S2 on insulin resistance, and determine whether the insulin resistance in mice fed a high-fat diet (HFD) results from G0S2 elevation.

Association between Regional Body Muscle Mass and Non-Alcoholic Fatty Liver Disease: An Observational Study Using Data from the REACTION Study.

Regional muscle distribution is associated with abdominal obesity and metabolic syndrome. However, the relationship between muscle distribution and nonalcoholic fatty liver disease (NAFLD) remains unclear. This study was to determine the relationship between regional muscle distribution and the risk and severity of NAFLD.

Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction.

Diabetes-associated cognitive decline (DCD), is one of the complications of diabetes, which is characterized by a series of neurophysiological and pathological abnormalities. However, the exact pathogenesis of DCD is still unknown. Single-cell RNA sequencing (scRNA-seq) could discover unusual subpopulations, explore functional heterogeneity and identify signaling pathways and potential markers.

Relationship between plasma 12,13-diHOME level and nonalcoholic fatty liver disease in patients with type 2 diabetes and obesity.

Background: 12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) was one of the newly found lipokines. The goal of this study was to investigate whether the 12,13-diHOME was associated with related metabolic markers of nonalcoholic fatty liver disease (NAFLD) in a Chinese population with type 2 diabetes (T2DM) and obesity.

Methods: This cross-sectional study enrolled 202 subjects with T2DM.

Statin Use and Benefits of Thyroid Function: A Retrospective Cohort Study.

Purpose: Previous studies have suggested that cholesterol may influence thyroid function. Since statins are widely used for their cholesterol-lowering effect, we aimed to assess the association between statin use and thyroid function, and also to explore the role of the cholesterol-lowering effect in it.

Methods: We performed a retrospective cohort study derived from REACTION study.

Pharmacological Inhibition of Galectin-3 Ameliorates Diabetes-Associated Cognitive Impairment, Oxidative Stress and Neuroinflammation in vivo and in vitro.

Background: In diabetes, cognitive impairment is linked with oxidative stress and neuroinflammation. As the only chimeric member of the galectin family, galectin-3 (Gal3) induces neuroinflammation and cognitive impairment in models of Alzheimer's disease (AD); however, its role in diabetes-associated cognitive impairment is not established.

Methodology: Here, we investigated the effects of Gal3 inhibition on cognitive impairment and the possible underlying molecular events in diabetes.

TSH promotes adiposity by inhibiting the browning of white fat.

Adiposity is caused by an imbalance between energy intake and consumption. Promotion of the browning of white fat increases energy expenditure and could combat adiposity. Thyroid-stimulating hormone (TSH) has been confirmed to positively correlate with adiposity.

Gut dysbiosis is associated with primary hypothyroidism with interaction on gut-thyroid axis.

Background Previous studies have shown that the gut microbiome is associated with thyroid diseases, including Graves' disease, Hashimoto's disease, thyroid nodules, and thyroid cancer. However, the association between intestinal flora and primary hypothyroidism remains elusive. We aimed to characterize gut microbiome in primary hypothyroidism patients.

FSHR ablation induces depression-like behaviors.

Alteration in reproductive hormones profile is associated with the increasing risk of menopausal depression in women. Serum follicle-stimulating hormone (FSH) level is changed during the menopause transition, while the effect of FSH on menopausal depression has remained undefined. In this study we investigated whether or how FSH affected menopausal depression in postmenopausal (ovariectomized) FSHR knockout mice (Fshr).

Prevalence of mild cognitive impairment in type 2 diabetes mellitus is associated with serum galectin-3 level.

Aims/introduction: Galectin-3 (Gal3) contributes to insulin resistance, inflammation and obesity, the three risk factors for mild cognitive impairment (MCI) in type 2 diabetes mellitus patients.

Materials And Methods: A total of 134 hospitalized type 2 diabetes mellitus patients were assessed by the Montreal Cognitive Assessment method, and divided into 65 MCI and 69 controls. Levels of variables, Gal3 and Aβ42, were investigated in relation with cognitive function in both type 2 diabetes mellitus patients with MCI and high-fat diet/streptozotocin induced type 2 diabetes mellitus rats.

Therapeutic targets of hypercholesterolemia: HMGCR and LDLR.

Cholesterol homeostasis is critical and necessary for the body's functions. Hypercholesterolemia can lead to significant clinical problems, such as cardiovascular disease (CVD). 3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) and low-density lipoprotein cholesterol receptor (LDLR) are major points of control in cholesterol homeostasis.

Fenofibrate-induced hepatotoxicity: A case with a special feature that is different from those in the LiverTox database.

What Is Known And Objective: We report a special case of fenofibrate-induced acute severe DILI with sudden onset and rapid recovery, which is different from those in the LiverTox database.

Case Summary Description: The acute severe DILI occurred within only 4 days after fenofibrate initial treatment for hypertriglyceridemia. Liver enzyme levels eventually declined to normal within two weeks after the discontinuation of fenofibrate.

SREBP-2, a new target of metformin?

Background: Metformin, as the first-line treatment anti-diabetic drug, represents increasing evidence of a potential efficacy in improving dyslipidemia. However, the exact molecular mechanism(s) by which metformin influences lipid metabolism remains incompletely understood.

Methods: The HepG2 cells were treated with metformin and the AMP-activated protein kinase (AMPK) inhibitor compound C or a dominant-negative form of AMPK plasmid.

Amelioration of hepatic steatosis is associated with modulation of gut microbiota and suppression of hepatic miR-34a in (Thunb.) Makino treated mice.

Background: Non-alcoholic fatty liver disease (NAFLD) is a chronic and progressive liver disease with an increased risk of morbidity and mortality. However, so far no specific pharmacotherapy has been approved. (Thunb.

Role of exosome-associated microRNA in diagnostic and therapeutic applications to metabolic disorders.

Metabolic disorders are classified clinically as a complex and varied group of diseases including metabolic syndrome, obesity, and diabetes mellitus. Fat toxicity, chronic inflammation, and oxidative stress, which may change cellular functions, are considered to play an essential role in the pathogenetic progress of metabolic disorders. Recent studies have found that cells secrete nanoscale vesicles containing proteins, lipids, nucleic acids, and membrane receptors, which mediate signal transduction and material transport to neighboring and distant cells.

Thyroid stimulating hormone increases hepatic gluconeogenesis via CRTC2.

Epidemiological evidence indicates that thyroid stimulating hormone (TSH) is positively correlated with abnormal glucose levels. We previously reported that TSH has direct effects on gluconeogenesis. However, the underlying molecular mechanism remains unclear.