IBS and FD were the

most frequent combinations in overlapping FGID. Most cases of FD are possibly parts of functional bowel disorders. “
“Department of Endocrinology, People’s Hospital of Gansu Province Department of Endocrinology, Shandong Provincial Qianfoshan Hospital, Jinan, China Elevated thyroid-stimulating hormone (TSH) and hypercholesterolemia commonly coexist, as typically seen in hypothyroidism, but there is no known mechanism directly linking the two. Here, we demonstrated that in liver cells, TSH promoted the expression of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR), a rate-limiting enzyme in cholesterol synthesis, by acting on the TSH receptor in hepatocyte membranes and stimulating the cyclic adenosine monophosphate / protein kinase A / cyclic adenosine monophosphate–responsive element binding protein (cAMP/PKA/CREB) signaling system. In thyroidectomized

rats, the production of endogenous thyroid CP673451 hormone was eliminated and endogenous TSH was suppressed through pituitary suppression with constant administration of exogenous thyroid hormone, and hepatic HMGCR expression was increased by administration of exogenous TSH. These results suggested that TSH could up-regulate hepatic HMGCR expression, which indicated a potential mechanism see more for hypercholesterolemia involving direct action of TSH on the liver. (HEPATOLOGY 2010) Hypothyroidism is well known to be associated with elevated serum TC, which can result in hypercholesterolemia.1, 2 The underlying mechanism is widely thought to be TH deficiency. However, elevation of serum TC has also been observed in patients Thiamine-diphosphate kinase with subclinical hypothyroidism (SCH), in which TSH is elevated but TH stays within its normal range.1, 3, 4 Thus, the development of hypercholesterolemia in SCH cannot be explained only by the role of TH. This raises the question of whether elevated TSH also plays a role in the development of hypercholesterolemia in hypothyroidism. Several clinical studies in recent years addressed this issue

and showed a correlation in hypothyroidism between high serum cholesterol and high TSH levels, the latter being usually used as an indication of the severity of the hypothyroidism.5-7 In these studies, however, it was impossible to delineate a direct role of TSH as abnormal TH level (usually deficiency) was usually a coexisting factor. Thus, a molecular mechanism by which TSH might affect cholesterol level has never been established. The TSHR is expressed in thyroid cells and plays a central role in up-regulating its function, including the synthesis of TH. Increasing data showed that the TSHR was also expressed in many nonthyroid tissues, and it might actually play a physiological role in these tissues.8, 9 We recently demonstrated that TSHR was expressed in hepatocytes and that stimulation of cultured liver cells with TSH increased the production of cAMP.