The role of thyroid hormone in metabolism and metabolic syndrome

Abstract

Metabolic syndrome (MetS) and thyroid dysfunction are common in clinical practice. The objectives of this review are to discuss some proposed mechanisms by which thyroid dysfunctions may lead to MetS, to describe the bidirectional relationship between thyroid hormones (THs) and adiposity and finally, to resume a list of recent studies in humans that evaluated possible associations between thyroid hormone status and MetS or its clinical components. Not solely THs, but also its metabolites regulate metabolic rate, influencing adiposity. The mechanisms enrolled are related to its direct effect on adenosine triphosphate (ATP) utilization, uncoupling synthesis of ATP, mitochondrial biogenesis, and its inotropic and chronotropic effects. THs also act controlling core body temperature, appetite, and sympathetic activity. In a bidirectional way, thyroid function is affected by adiposity. Leptin is one of the hallmarks, but the pro-inflammatory cytokines and also insulin resistance impact thyroid function and perhaps its structure. MetS development and weight gain have been positively associated with thyroid-stimulating hormone (TSH) in several studies. Adverse glucose metabolism may be related to hyperthyroidism, but also to reduction of thyroid function or higher serum TSH, as do abnormal serum triglyceride levels. Hypo- and hyperthyroidism have been related to higher blood pressure (BP), that may be consequence of genomic or nongenomic action of THs on the vasculature and in the heart. In summary, the interaction between THs and components of MetS is complex and not fully understood. More longitudinal studies controlling each of all confounding variables that interact with endpoints or exposure factors are still necessary.

The Role of Thyroid Hormones and Autoantibodies in Metabolic Dysfunction Associated Fatty Liver Disease: TgAb May Be a Potential Protective Factor

“…Thyroid hormones (THs) play a fundamental role in metabolism. Thyroid dysfunction is considered to be associated with type 1 diabetes mellitus (T1DM), T2DM ( 7 ), and metabolic syndrome (MetS) ( 8 ). THs targets the liver to regulate body weight, lipogenesis, lipid metabolism, and insulin resistance (IR).…”

Hypothyroidism-Induced Nonalcoholic Fatty Liver Disease (HIN): Mechanisms and Emerging Therapeutic Options

“…NAFLD subjects have high levels of diacylglycerols, triacylglycerols, and elevated saturated FAs composition. Triacylglycerol can accumulate as fat droplets, or can be added to very-low-density lipoprotein (VLDL) or help with cellular reparation [ 108 , 109 ]. It seems that the derivative 3,5-diiodothyronine can regulate the activity of hepatic lipases to raise lipid mobilization from fat droplets [ 110 ].…”

“…TH indirectly drives the transcriptional regulation of liver lipogenesis as a result of its effect on carbohydrate-responsive element-binding protein (ChREBP) and liver X receptors. They can lower the VLDL, LDL, high-density lipoproteins (HDL), and apolipoprotein B100 levels [ 109 ]. TH can lower LDL by reducing the proprotein convertase subtilisin/kexin type 9 (PCSK9) levels.…”

Glucose Metabolism, Thyroid Function, and Prolactin Level in Adolescent Patients With First Episode of Schizophrenia and Affective Disorders

“…Moreover, higher PRL levels have been found in first episode drug-naïve psychotic patients compared to healthy controls; further researches are needed to clarify the relationship between stress, HPRL, and emergence of the psychotic symptoms, also considering the role of confounding factors as age, sex, body mass index (BMI), and thyroid stimulating hormone (26)(27)(28). Thyroid dysfunctions are frequently associated in clinical practice with metabolic syndrome (29,30) as well as a relationship exists between HPRL and hypothyroidism, also in children (31). In addition, altered hypothalamic-pituitary-thyroid system's function has been described in schizophrenia, bipolar and depressive disorders (32)(33)(34), but very few studies have been conducted at the onset of these illnesses (1,35).…”