Hormone Interactions with Receptors

By Dr Ananya Mandal, MD

Hormones are chemical messengers that interact with receptors present on the surface of a cell membrane or with receptors that are located inside the cell, in the cytoplasm (cytoplasmic receptors). This interaction gives rise to the effects hormones exert on target cells and organs.

Hormones are secreted by the endocrine glands, which do not have ducts and secrete the hormones directly into the local blood stream which carries them to the various different tissues and organs in the body.

Types of hormone

Different types of hormones have varying chemical structures. While some are peptides or proteins composed of amino acids, others are steroid hormones derived from lipids. Some peptide hormones include a covalently attached oligosaccharide, in which case they are termed glycoproteins. The different chemical structures of varying types of hormones means they all have receptors with a specific shape, size and function.

Water-soluble hormones

Most water-soluble hormones such as glycoproteins and peptides combine with a receptor present on the plasma membrane because they are not lipid soluble and cannot move through the phospholipid cell membrane. As these hormone binds to their receptor, a cascade of reactions is triggered within the cytoplasm of the cell.

The integral membrane receptors usually function through the activation of secondary messengers inside the plasma membrane which carry out intracellular signal transduction to convey the effects of the hormones that cannot enter the cells.

Lipid soluble receptors

Receptors for lipid-soluble hormones such as the steroid hormones estrogen and thyroxine lie within the cytoplasm. These hormones need to enter the cell by crossing the cell membrane. Once bound, the hormone-receptor complex moves into the nucleus where it binds to specific DNA sequences and acts as a transcription factor, either increasing or suppressing the expression of certain genes.

Reviewed by , BSc

Further Reading

Last Updated: Dec 2, 2013

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