0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Gallstone Disease and Its Correlation With Thyroid Disorders: A Narrative Review

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Over the years, several studies have revealed an important link between thyroid disorders and gallstone disease. According to these studies, hypothyroidism and hyperthyroidism are associated with cholesterol gallstone disease. This association between thyroid hormone disorders and cholesterol gallstone disease is due to the importance of thyroid hormones on cholesterol synthesis, bile functioning and content, and gallbladder motility. Several genes and receptors have been found on the thyroid gland, liver, and gallbladder to verify this association. These genes affect thyroid hormone secretion, lipid metabolism, and bile secretion. Defects in these various gene expression and protein functions lead to bile duct diseases. Other causes that lead to cholesterol gallstone disease are supersaturation of the bile with cholesterol and impaired gallbladder motility, which leads to bile stasis. This article has discussed these factors in detail while highlighting the association between thyroid hormones and cholesterol gallstone disease. 

          Related collections

          Most cited references122

          • Record: found
          • Abstract: found
          • Article: not found

          Identification of a nuclear receptor for bile acids.

          Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Physiological and molecular basis of thyroid hormone action.

            P M Yen (2001)
            Thyroid hormones (THs) play critical roles in the differentiation, growth, metabolism, and physiological function of virtually all tissues. TH binds to receptors that are ligand-regulatable transcription factors belonging to the nuclear hormone receptor superfamily. Tremendous progress has been made recently in our understanding of the molecular mechanisms that underlie TH action. In this review, we present the major advances in our knowledge of the molecular mechanisms of TH action and their implications for TH action in specific tissues, resistance to thyroid hormone syndrome, and genetically engineered mouse models.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation.

              While bile acids (BAs) have long been known to be essential in dietary lipid absorption and cholesterol catabolism, in recent years an important role for BAs as signalling molecules has emerged. BAs activate mitogen-activated protein kinase pathways, are ligands for the G-protein-coupled receptor (GPCR) TGR5 and activate nuclear hormone receptors such as farnesoid X receptor alpha (FXR-alpha; NR1H4). FXR-alpha regulates the enterohepatic recycling and biosynthesis of BAs by controlling the expression of genes such as the short heterodimer partner (SHP; NR0B2) that inhibits the activity of other nuclear receptors. The FXR-alpha-mediated SHP induction also underlies the downregulation of the hepatic fatty acid and triglyceride biosynthesis and very-low-density lipoprotein production mediated by sterol-regulatory-element-binding protein 1c. This indicates that BAs might be able to function beyond the control of BA homeostasis as general metabolic integrators. Here we show that the administration of BAs to mice increases energy expenditure in brown adipose tissue, preventing obesity and resistance to insulin. This novel metabolic effect of BAs is critically dependent on induction of the cyclic-AMP-dependent thyroid hormone activating enzyme type 2 iodothyronine deiodinase (D2) because it is lost in D2-/- mice. Treatment of brown adipocytes and human skeletal myocytes with BA increases D2 activity and oxygen consumption. These effects are independent of FXR-alpha, and instead are mediated by increased cAMP production that stems from the binding of BAs with the G-protein-coupled receptor TGR5. In both rodents and humans, the most thermogenically important tissues are specifically targeted by this mechanism because they coexpress D2 and TGR5. The BA-TGR5-cAMP-D2 signalling pathway is therefore a crucial mechanism for fine-tuning energy homeostasis that can be targeted to improve metabolic control.
                Bookmark

                Author and article information

                Journal
                Cureus
                Cureus
                2168-8184
                Cureus
                Cureus (Palo Alto (CA) )
                2168-8184
                12 September 2023
                September 2023
                : 15
                : 9
                : e45116
                Affiliations
                [1 ] Medicine and Surgery, SVS Medical College, Mahabubnagar, IND
                [2 ] Internal Medicine, Sri Padmavathi Medical College for Women, Sri Venkateswara Institute of Medical Sciences (SVIMS), Tirupati, IND
                [3 ] Internal Medicine, Punjab Institute of Medical Sciences, Jalandhar, IND
                [4 ] Medicine and Surgery, AMA School of Medicine, Makati, PHL
                [5 ] Medicine and Surgery, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, IND
                [6 ] Medicine, St. John’s Medical College Hospital, Rajiv Gandhi University of Health Sciences (RGUHS), Bengaluru, IND
                [7 ] Medicine and Surgery, Obafemi Awolowo University, Ile-Ife, NGA
                [8 ] Medicine and Surgery, Jackson Memorial Hospital, Miami, USA
                [9 ] Medicine and Surgery, Shendi University, Shendi, SDN
                [10 ] Medicine and Surgery, Government Medical College Kottayam, Kottayam, IND
                [11 ] Neurosurgery, Mayo Hospital, Lahore, PAK
                Author notes
                Article
                10.7759/cureus.45116
                10568238
                37842424
                85febd36-9292-449d-bbf4-fced4c762929
                Copyright © 2023, Ravi et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 8 July 2023
                : 12 September 2023
                Categories
                Internal Medicine
                Medical Education
                Gastroenterology

                gallstones,hyperthyroidism,hypothyroidism,thyroid disorder,cholelithiasis

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content759

                Cited by3

                Most referenced authors1,659