Endocrinology and Metabolic Disease


Introduction of endocrinology and metabolism

Endocrinology is the study of communication and control within a living organism by means of chemical messengers that are synthesized in whole or in part by that organism. Metabolism, an integral part of the science of endocrinology, is the study of the biochemical control mechanisms that occur within living organisms. The term includes such diverse activities as gene express; biosynthetic pathways and their enzymatic catalysis; the modification, transformation, and degradation of biologic substances; the biochemical mediation of the actions and interactions of such substances; and the means for obtaining, storing, and mobilizing energy. The chemical messengers of endocrinology are the hormones, endogenous informational molecules that are involved in both intracellular and extracellular communication. Endocrinology and metabolism are broad subjects that incorporate much, if not all, of normal body functions and disease states, they defy easy categorization. Endocrine and metabolic diseases span a vast range of conditions. Together, they affect many millions of persons and can profoundly decrease quality of life.

Endocrine Disorders

Endocrine disorders involve an abnormality of one of the body’s endocrine glands.

Thyroid under-activity/over-activity: Of the endocrine disorders, thyroid diseases are the most common. Effective treatment of thyroid over-activity (hyperthyroidism) and under-activity (hypothyroidism) is important in both the short term and long term. Although treating underactive thyroid is a bit more complex, either condition can be treated effectively.

Thyroid growths: Most thyroid growths do not have serious consequences. A technique called “fine-needle aspiration” can be used to identify the minority of thyroid growths that are cancerous. The technique involves insertion of a small needle into the thyroid growth and withdrawing a small amount of fluid-much like drawing a blood sample from a vein. Cells in that fluid are then examined under a microscope.

Other endocrine disorders: Disorders of the other endocrine glands are less common. The expertise of an endocrinologist often is needed to select the most efficient diagnostic approach, assess the need for treatment, select the best treatment approach, and assure a favorable outcome.

Many endocrine disruptive chemicals (EDCs) have similar structures to NR ligands and can directly bind to NRs. They can either act as agonists and induce gene expression or function as antagonists and inhibit the activity of the receptor. In addition, enzymes induced by activated aryl hydrocarbon receptor (AhR) are not only involved in metabolism of xenobiotics but also in the catabolism of steroid hormones. Thus, induction of these enzymes can lead to reduced availability of endogenous hormones.

Metabolic Disorders

The metabolic syndrome (visceral obesity, diabetes mellitus, dyslipidaemia, hyperglycaemia, and hypertension), has become one of the major public-health challenges worldwide. There has been growing interest in this constellation of closely related risk factors.

Obesity: Obesity is associated with chronic activation of inflammatory pathways in both adipocytes and in macrophages residing in or infiltrating the adipose tissue. Adipocytes are not only lipid storage depots, but also secretory cells that produce proinflammatory cytokines and adipokines. Adipocytes monitor energy storage levels and release proinflammatory cytokines to report overnutrition to the rest of the body. Adipocytes from obese mice produce the chemokines and cytokines such as MCP-1, MIPs, IL-6, IL-1β, and TNF-α. A finding consistent with increased CD8 cells in obese human patients indicated that cytotoxic T lymphocytes of the CD8 lineage are greatly enriched in the adipose tissue of mice fed a diet high in fat.

Diabetes mellitus: Diabetes mellitus is the most common endocrine/metabolic disorder, which has been viewed historically as lipid storage disorders brought about by overnutrition. It is more common as we age and is more prevalent in African Americans, Latinos and Native Americans. Type Ⅱ diabetes begins with insulin resistance, the impaired responsiveness of target organs to circulating insulin. As β cells in the pancreas work to produce more and more insulin, metabolic stress signals recruit monocytes to clear dying β cells. These recruited monocytes differentiate into TNF-α, IL-6, and IL-1 producing macrophages that promote further β cell dysfunction and death. Studies of genetic mutant mice demonstrate an essential role for NF-κB in the inflammatory response required for the development of insulin resistance.


Recent research shows that there is indeed a potential risk that endocrine and metabolic disruptors can induce human metabolic disorders, but they also illustrate that there is a lot more information needed to link molecular and toxicological/epidemiological information. The dramatic increase in obesity, in particular childhood obesity, shows that prevention and intervention actions are needed urgently. However, the complexity in the etiology of obesity and metabolic syndrome, in combination with the diversity of the endocrine systems involved, calls for more scientific research and information.

As one of the world leading suppliers of chemical reagents and kinase inhibitors, BOC Sciences has directed sincere efforts toward providing customers with high quality small molecule reagents for endocrine and metabolic disease research. Besides, BOC Sciences can provide the related impurities and metabolites to our customers for research.


  1. Frohman, L. A. (2001). Endocrinology and metabolism (p. 627). P. Felig (Ed.). New York, NY: McGraw-Hill.
  2. Grundy, S. M. (2004). Obesity, metabolic syndrome, and cardiovascular disease. The Journal of Clinical Endocrinology & Metabolism89(6), 2595-2600.
  3. Wulsin, L. R., Horn, P. S., Perry, J. L., Massaro, J. M., & D'agostino, R. B. (2015). Autonomic imbalance as a predictor of metabolic risks, cardiovascular disease, diabetes, and mortality. The Journal of Clinical Endocrinology & Metabolism100(6), 2443-2448.