scholarly journals Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction?

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Gabriela Brenta
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Thyroid Hormone ◽  
Glucose Metabolism ◽  
Thyroid Hormones ◽  
Thyroid Dysfunction ◽  
Natural Consequence ◽  
Apparent Paradox ◽  
Peripheral Tissues ◽  
Differential Effects

Evidence for a relationship between T4 and T3 and glucose metabolism appeared over 100 years ago when the influence of thyroid hormone excess in the deterioration of glucose metabolism was first noticed. Since then, it has been known that hyperthyroidism is associated with insulin resistance. More recently, hypothyroidism has also been linked to decreased insulin sensitivity. The explanation to this apparent paradox may lie in the differential effects of thyroid hormones at the liver and peripheral tissues level. The purpose of this paper is to explore the effects of thyroid hormones in glucose metabolism and analyze the mechanisms whereby alterations of thyroid hormones lead to insulin resistance.

Central versus peripheral impact of estradiol on the impaired glucose metabolism in ovariectomized mice on a high-fat diet

2012 ◽  
Vol 303 (4) ◽  
pp. E445-E456 ◽  
Author(s):  
Rika Yonezawa ◽  
Tsutomu Wada ◽  
Natsumi Matsumoto ◽  
Mayuko Morita ◽  
Kanae Sawakawa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Peripheral Tissues ◽  
Ovariectomized Mice ◽  
Brown Adipose ◽  
Peripheral Actions

Age-related loss of ovarian function promotes adiposity and insulin resistance in women. Estrogen (E2) directly enhances insulin sensitivity and suppresses lipogenesis in peripheral tissues. Recently, the central actions of E2 in the regulation of energy homeostasis are becoming clearer; however, the functional relevance and degree of contribution of the central vs. peripheral actions of E2 are currently unknown. Therefore, we prepared and analyzed four groups of mice. 1) Control: sham-operated mice fed a regular diet, 2) OVX-HF: ovariectomized (OVX) mice fed a 60% high-fat diet (HF), 3) E2-SC: OVX-HF mice subcutaneously treated with E2, and 4) E2-ICV: OVX-HF mice treated with E2 intracerebroventricularly. OVX-HF mice showed increased body weight with both visceral and subcutaneous fat volume enlargement, glucose intolerance, and insulin resistance. Both E2-SC and E2-ICV equally ameliorated these abnormalities. Although the size of adipocytes and number of CD11c-positive macrophages in perigonadal fat in OVX-HF were reduced by both E2 treatments, peripherally administered E2 decreased the expression of TNFα, lipoprotein lipase, and fatty acid synthase in the white adipose tissue (WAT) of OVX-HF. In contrast, centrally administered E2 increased hormone-sensitive lipase in WAT, decreased the hepatic expression of gluconeogenic enzymes, and elevated core body temperature and energy expenditure with marked upregulation of uncoupling proteins in the brown adipose tissue. These results suggest that central and peripheral actions of E2 regulate insulin sensitivity and glucose metabolism via different mechanisms, and their coordinated effects may be important to prevent the development of obesity and insulin resistance in postmenopausal women.

scholarly journals Differential effects of glucagon-like peptide-1 on microvascular recruitment and glucose metabolism in short- and long-term insulin resistance

2015 ◽  
Vol 593 (9) ◽  
pp. 2185-2198 ◽  
Author(s):  
Kim A. Sjøberg ◽  
Stephen Rattigan ◽  
Jacob F. Jeppesen ◽  
Anne-Marie Lundsgaard ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Differential Effects ◽  
Short And Long Term ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Microvascular Recruitment

Pathophysiology and management of functional endocrine tumours in the critically ill

2016 ◽  
Author(s):  
Sara Nikravan ◽  
Frederick Mihm
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Diagnostic Tests ◽  
Concurrent Treatment ◽  
Peripheral Tissues ◽  
Endocrine Tumours ◽  
Optimal Dosing ◽  
Serum Thyroid Hormone ◽  
Thyroid Hormone Levels ◽  
T3 Receptors

Thyroid hormones act on most tissues via nuclear T3 receptors. Thyroid hormones stimulate oxygen consumption and heat production, influence cell growth and maturation (central nervous system, bone), and modulate metabolism (carbohydrates, lipids, proteins, drugs). Treatment for presumed thyroid disease frequently has to be initiated before the results of diagnostic tests are available. Treatment of hyperthyroidism should result in the reduction of serum thyroid hormone levels and their action on peripheral tissues with concurrent treatment of the precipitating event. In severe hypothyroidism the choice of thyroid hormone (thyroxine or tri-iodothyronine), optimal dosing, and the route of administration remain controversial

scholarly journals Role of Cannabinoid Receptor Type 1 in Insulin Resistance and Its Biological Implications

2019 ◽  
Vol 20 (9) ◽  
pp. 2109 ◽  
Author(s):  
Arulkumar Nagappan ◽  
Jooyeon Shin ◽  
Myeong Ho Jung
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Hepatic Steatosis ◽  
Cannabinoid Receptor ◽  
Inflammatory Responses ◽  
Hepatic Insulin Resistance ◽  
Leptin Resistance ◽  
Peripheral Tissues

Endogenous cannabinoids (ECs) are lipid-signaling molecules that specifically bind to cannabinoid receptor types 1 and 2 (CB1R and CB2R) and are highly expressed in central and many peripheral tissues under pathological conditions. Activation of hepatic CB1R is associated with obesity, insulin resistance, and impaired metabolic function, owing to increased energy intake and storage, impaired glucose and lipid metabolism, and enhanced oxidative stress and inflammatory responses. Additionally, blocking peripheral CB1R improves insulin sensitivity and glucose metabolism and also reduces hepatic steatosis and body weight in obese mice. Thus, targeting EC receptors, especially CB1R, may provide a potential therapeutic strategy against obesity and insulin resistance. There are many CB1R antagonists, including inverse agonists and natural compounds that target CB1R and can reduce body weight, adiposity, and hepatic steatosis, and those that improve insulin sensitivity and reverse leptin resistance. Recently, the use of CB1R antagonists was suspended due to adverse central effects, and this caused a major setback in the development of CB1R antagonists. Recent studies, however, have focused on development of antagonists lacking adverse effects. In this review, we detail the important role of CB1R in hepatic insulin resistance and the possible underlying mechanisms, and the therapeutic potential of CB1R targeting is also discussed.

scholarly journals Insulin and Insulin Resistance in Alzheimer’s Disease

2021 ◽  
Vol 22 (18) ◽  
pp. 9987
Author(s):  
Aleksandra Sędzikowska ◽  
Leszek Szablewski
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Cell Growth ◽  
Glucose Metabolism ◽  
Insulin Signaling ◽  
Brain Aging ◽  
Mapk Pathway ◽  
Metabolic Effects ◽  
Peripheral Tissues

Insulin plays a range of roles as an anabolic hormone in peripheral tissues. It regulates glucose metabolism, stimulates glucose transport into cells and suppresses hepatic glucose production. Insulin influences cell growth, differentiation and protein synthesis, and inhibits catabolic processes such as glycolysis, lipolysis and proteolysis. Insulin and insulin-like growth factor-1 receptors are expressed on all cell types in the central nervous system. Widespread distribution in the brain confirms that insulin signaling plays important and diverse roles in this organ. Insulin is known to regulate glucose metabolism, support cognition, enhance the outgrowth of neurons, modulate the release and uptake of catecholamine, and regulate the expression and localization of gamma-aminobutyric acid (GABA). Insulin is also able to freely cross the blood–brain barrier from the circulation. In addition, changes in insulin signaling, caused inter alia insulin resistance, may accelerate brain aging, and affect plasticity and possibly neurodegeneration. There are two significant insulin signal transduction pathways: the PBK/AKT pathway which is responsible for metabolic effects, and the MAPK pathway which influences cell growth, survival and gene expression. The aim of this study is to describe the role played by insulin in the CNS, in both healthy people and those with pathologies such as insulin resistance and Alzheimer’s disease.

scholarly journals Influence of Tacrolimus on Glucose Metabolism before and after Renal Transplantation: A Prospective Study

2001 ◽  
Vol 12 (3) ◽  
pp. 583-588 ◽  
Author(s):  
ELLY M. VAN DUIJNHOVEN ◽  
JOHANNES M. M. BOOTS ◽  
MAARTEN H. L. CHRISTIAANS ◽  
BRUCE H. R. WOLFFENBUTTEL ◽  
JOHANNES P. VAN HOOFF
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Sensitivity Index ◽  
Intravenous Glucose ◽  
Prospective Longitudinal Study ◽  
C Peptide ◽  
Before And After ◽  
Prospective Longitudinal

Abstract. Most studies concerning the influence of tacrolimus on glucose metabolism have been performed either in animals or after organ transplantation. These clinical studies have largely been transversal with patients who were using steroids. Therefore, this prospective, longitudinal study investigated the influence of tacrolimus on glucose metabolism before and after transplantation. Eighteen Caucasian dialysis patients underwent an intravenous glucose tolerance test before and 5 d after the start of tacrolimus. Insulin sensitivity index (kG), insulin resistance (insulin/glucose ratio and homeostasis model assessment), and C-peptide and insulin secretion were calculated. Trough levels of tacrolimus were measured. After transplantation, the occurrence of posttransplantation diabetes mellitus (PTDM) was prospectively monitored. Statistical analysis was performed using the Wilcoxon signed ranks test and Spearman's rho for correlation. Before tacrolimus, kG was indeterminate in three patients. During tacrolimus, kG decreased in 16 of 18 patients, from a median of 1.74 mmol/L per min to 1.08 mmol/L per min (P < 0.0001). The correlation between C-peptide and insulin data was excellent. Insulin secretion decreased from 851.0 mU × min/L to 558.0 mU × min/L (P = 0.014), whereas insulin resistance did not change. Insulin sensitivity correlated negatively with tacrolimus trough level. After transplantation, three patients developed PTDM; before tacrolimus, two had an indeterminate and one a low normal kG. During tacrolimus administration, kG decreased in almost all patients as a result of a diminished insulin secretion response to a glucose load, whereas insulin resistance did not change. Patients with an abnormal or indeterminate kG seem to be at risk of developing PTDM while on tacrolimus.

scholarly journals Metabolic Systemic Effects Triiodothyronine

2020 ◽  
Vol 10 (4) ◽  
pp. 262-271
Author(s):  
E. A. Troshina ◽  
E. S. Senyushkina
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Depressive Disorders ◽  
Vital Role ◽  
The Body ◽  
Metabolic Effects ◽  
Metabolic Efficiency ◽  
Peripheral Tissues ◽  
Activation Of Transcription ◽  
Genes Encoding

Triiodothyronine (T3, 3,5,3’-L-triiodothyronine) is a thyroid hormone (thyroid), the secretion of which is carried out directly both by the gland (to a lesser extent) and outside it (the main amount; as a result of peripheral deiodination of thyroxine (T4)). Getting into the nuclei of cells, T3 interacts with specific nuclear receptors of target tissues, which determines its biological activity. This interaction leads to the activation of transcription of a number of genes.In the pituitary gland and peripheral tissues, the action of thyroid hormones is modulated by local deiodinases, which convert T4 to more active T3, the molecular effects of which in individual tissues depend on subtypes of T3 receptors and their interaction with other ligands, coactivators and corepressors, as well as on the activation or repression of specific genes.The reason for the lack of T3 production is primarily a deficiency of iodine in the diet, less often, a defect in the genes encoding the proteins that are involved in T3 biosynthesis. As a result of the low intake of iodide in the body, the so-called adaptive mechanism is activated, which consists in increasing the proportion of synthesized T3, which increases the metabolic efficiency of thyroid homones. With a deficiency in the diet of such a trace element as selenium, the conversion of T4 to T3 is reduced.Thyroid hormones play a vital role in the regulation of homeostasis and the metabolic rate of cells and tissues of humans and mammals. They are necessary for physical and mental development. Their insufficient production at the stage of formation of the internal organs of the fetus and in childhood can lead to various pathologies, primarily to pathology of the central nervous system, and as a result, growth retardation and mental retardation. In adulthood, hypothyroidism leads to a decrease in metabolism, memory impairment, depressive disorders, impaired fertility. Many discussions and ambiguous conclusions have been obtained regarding combination drugs (sodium levothyroxine + lyothironon) for the treatment of hypothyroidism. This article will examine the metabolic effects of T3, the thyroid hormone with the highest activity. 

scholarly journals Adverse Effects of Bisphenol A Exposure on Glucose Metabolism Regulation

2016 ◽  
Vol 10 (1) ◽  
pp. 122-130 ◽  
Author(s):  
Ciro Menale ◽  
Damiano G. Mita ◽  
Nadia Diano ◽  
Sabrina Diano
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Adverse Effects ◽  
Bisphenol A ◽  
Estrogenic Activity ◽  
Endocrine Function ◽  
Peripheral Tissues ◽  
Metabolism Regulation

Bisphenol A (BPA) is used as basic chemical compound in the production of polycarbonate food containers or epoxy resins coating metallic cans for food and beverages conservation. Its xeno-estrogenic activity alters endocrine-metabolic pathways modulating glucose metabolism and increasing the risk of developing diabetes, insulin resistance, and obesity. Based on in vitro and in vivo experimental research, here we report some of the major BPA adverse effects on tissues that play a key role in the regulation on the whole body’s metabolism. Evidences have shown that BPA is able to exert its endocrine disrupting action altering glucose metabolism and contributing to the onset of metabolic disorders, acting on liver functions and affecting insulin production by the pancreas. Exposure to BPA has been reported also to modulate glucose utilization in muscles, as well as to interfere with adipose tissue endocrine function. In addition, to peripheral tissues, recent studies have shown that BPA by acting in the Central Nervous System affects neuroendocrine regulation of glucose metabolism, promoting glucose metabolism dysfunction such as glucose intolerance and insulin resistance. Thus, exposure to BPA seems to be an important risk factor in the onset of obesity and metabolic syndrome. However, its mechanisms of action need to be further investigated to provide a major evaluation of risk assessment.

scholarly journals SAT-LB80 Elevated Pre-Op Thyrotropin Levels Are Associated With Increased 30-Day Mortality in Patients Undergoing Cardiac Surgery With Cardiopulmonary Bypass

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shariq Rashid Masoodi ◽  
Rameesa Batul ◽  
Khurram Maqbool ◽  
Amir Zahoor ◽  
Mona Sood ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Hormone Levels ◽  
Icu Stay ◽  
Thyroid Hormone Levels ◽  
Serum Thyroid Hormones

Abstract BACKGROUND: The association between thyroid dysfunction and postoperative mortality is contentious. Thyroid function is frequently depressed during and after cardiopulmonary bypass surgical procedures, and this may adversely affect myocardial performance and postop outcome.OBJECTIVES: To study i) the changes and clinical significance of serum thyroid hormones during cardiopulmonary bypass (CPB), and ii) the association between biochemically assessed peri-op thyroid function and 30-day mortality after CBPSTUDY DESIGN: Prospective Cohort StudySUBJECTS: 279 patients undergoing various cardiac surgeries under cardiopulmonary bypass.METHODS: All consenting patients undergoing open heart surgery in last five years at a tertiary care centre in North-India were studied. The thyroid hormone levels (Total T3, T4 and TSH) were measured before admission, and postoperatively on Day 1 & 7, and 3 months following surgery. The patients’ gender, age, weight, body mass index, heart disease details, previous cardiac surgeries, and cardiac surgery-related data such as pump time, aortic clamping time, hypothermia duration, postoperative hemodynamic status and postoperative use of inotropic drugs were recorded and analysed. Patients were classified as having biochemically overt or subclinical hyperthyroidism or hypothyroidism, normal thyroid function, or non-classifiable state based on preoperative thyroid-stimulating hormone and total T4 values. Outcome data were collected from hospital records. Biochemical thyroid dysfunction was not systematically treated. Outcomes measured were length of ICU stay, postoperative complications and 30-day mortality.RESULTS: There was significant changes in thyroid function in patients undergoing cardiopulmonary bypass surgery (Fig 1). All patients showed a decrease in T3, T4 and TSH after surgery. Post-op complications were observed in 137 patients (49%) most common being atrial fibrillation (34%) followed by acute kidney injury (23%), infections (18%), dyselectrolytemia (7%), bleeding (1.4%) and ARDS (1.4%). Of 263 patients followed, eventually 26 patients expired with a mortality rate of 8.89% (95% CI, 0.4 - 19.4). Perioperatively, there was a significant correlation between 30-day with type of surgery (r, 0.26), aortic clamp time (r, 0.45), CBP time (r, 0.48), number of inotropes used (r, 0.57), hours of mechanical ventilation (r, 0.4), ICU stay (r, 0.13) and post-op complications (r, 0.24), as well as with the reduction in the thyroid hormone levels; 17 (7%), 3 (20%) and 6 (46%) patients of those with pre-op TSH level of &lt;6.5, &gt;6.5 and &gt;10.5 mIU/L expired (p &lt;0.001).CONCLUSION: Pre-op thyroid dysfunction is associated with increased mortality in patients undergoing cardiac surgery with CBP. Excess mortality with elevated serum TSH levels suggests the importance of timely detection and intervention in individuals with thyroid dysfunction undergoing cardiac surgery.Table of Contents oTable 1. Characteristics of patients who expired versus those who survived cardiac surgery with cardiopulmonary bypass (CPB) oFig 1. Changes in serum thyroid hormones during CPB surgery oTable 1. Characteristics of patients who expired versus those who survived cardiac surgery with cardiopulmonary bypass (CPB) oFigures in parenthesis indicate ±Standard Deviation, unless indicated otherwise oFig 1. Changes in serum thyroid hormones during CPB surgery

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