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1、The Thyroid and CardioMetabolic CareMerck International Thyroid Symposium Rio de Janeiro, April 16 this action gives rise to the expression of UCP1 in brown fat and UCP3 in skeletal muscle and brown fat of mammals. The process of adaptation to cold is made by the hypothalamus activating the nervous
2、system for the secretion of norepinephrine promote UCP1 expression generated only in the mitochondria of brown fat. The uncoupling function of UCP1 is the oxide reduction in the phosphorylation of ADP. The decoupling does not occur without sympathetic stimulation but also occurs in the absence of th
3、yroid hormones. Further more, leptin and insulin are potent stimulators of the expression of UCP1 and thermogenesis in brown fat. UCP3 has an important role in regulating energy balance and lipid metabolism by its action in skeletal muscle. Gene expression to generate UCP3 in skeletal muscle is regu
4、lated by T3, the beta 3 adrenergic receptor agonists and leptin. The cold stimulates in brown fat mRNA expression of UCP3 as T3 and leptin. The increased expression of UCP3 is promoted by exercise, fasting and fatty acid concentration.9:3010:00 Influence of thyroid function on body weightSara Arella
5、no Montao, Mexico City, MexicoSession 1: The Thyroid and Metabolism Friday, April 16, 2010Changes in thyroid function result in alterations of lipoprotein metabolism. Thyroid hormones stimulate the gene expression and increase the amount and activities of some key enzymes involved in the lipogenic p
6、athway. Thyroid hormones stimulate the cholesterol synthesis by inducing the 3hydroxy3methyl glutarylcoenzyme A (HMGCoA) reductase, resulting in an increased intracellular cholesterol concentration in hyperthy roidism and a decreased one in hypothyroidism, and more specifically activated the low den
7、sity lipoprotein (LDL) receptors inducing the hepatic LDL mRNA receptor expression. Thyroid hormones also modulate the activity of cholesterolester transfer protein (CETP), an enzyme that transports cholesterol esters from high density lipoprotein 2 (HDL2) to the very low density lipoproteins (VLDL)
8、 and triglycerides in the opposite direction. Lastly, thyroid hormones stimulate the lipoprotein lipase (LPL), and the hepatic lipase (HL), that hydrolyzes HDL2 to HDL3. Overall, overt and subclinical hyperthyroidism is associated with a decrease in serum levels of cholesterol, LDL and HDL related t
9、o an increase in lecithin cholesterol acyl transferase and hepatic lipogenesis. In the transition from hyperthyroidism to euthyroidism few but significant changes are found. Overt and subclinical hypothyroidism is often accompanied by mild insulin resistance and an increase in serum cholesterol leve
10、ls, mainly due to elevation of LDL. These changes are positively related to TSH categories. In some patients elevated serum triglycerides and lipoproteina have been found whereas the HDL values are usually normal. These changes may increase the risk of accelerated atherosclerosis and premature coron
11、ary artery disease in some patients. Replacement therapy with levothyroxine usually improves the lipid profile, but in subclin ical hypothyroidism further studies are still necessary. 10:0010:30 Thyroid function and lipidsJoo Hamilton Romaldini, Campinas, BrazilThe Thyroid and CardioMetabolic Care F
12、inal Program and Abstracts 8 | 9It is well known that thyroid hormones regulate several pathways of glucose metabolism. These effects include modi fications of the circulating levels of insulin and counter regulatory hormones, and changes to intestinal absorption, hepatic production and peripheral t
13、issue uptake (fat and muscle) of glucose. Interestingly, thyroid hormones act differ entially on liver, skeletal muscle and adipose tissue, the main targets of insulin action. While thyroid hormones stimulate hepatic gluconeogenesis, they also stimulate insulinmediated glucose disposal in skeletal m
14、uscle and adipose tissue by several possible mechanisms, including an increase in GLUT4 transcription. Moreover, the hormonal message is modulated at a local level by a series of control steps, including the intracellular concentration of T3 via the deiodinases, and the relative concentration of T3
15、receptor isoforms, coactivators, and corepressors. These pathways are responsible for making tissues sensitive or resistant to the actions of thyroid hormone. It is not unexpected that overt thyroid disease exerts profound modifications in glucose homeostasis. Thyrotoxicosis has been related to gluc
16、ose intolerance and diabetic ketoacidosis. In severe hypothyroidism although a lower glucose disposal has been reported, liver glucose output remains unimpaired or decreased and this accounts for the diminished insulin require ment in diabetic patients with hypothyroidism. As regards subclinical hypo and hyperthyroidism, an association with insulin resistance has also been described. The prevalence of su
