Blood sugar regulation

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Ball-and-stick model of a glucose molecule

For homeostasis, insulin is the main hormone involved.

Blood sugar regulation is the process by which the levels of blood sugar, primarily glucose, are maintained by the body. Glucose regulation in the body is a process of keeping the body in homeostasis.

Mechanisms of blood sugar regulation

Blood sugar levels are regulated by negative feedback in order to keep the body in homeostasis. The levels of glucose in the blood are monitored by the cells in the pancreas's Islets of Langerhans.


If the blood glucose level falls to dangerous levels (as in very heavy exercise or lack of food for extended periods), the Alpha cells of the pancreas release glucagon, a hormone whose effects on liver cells act to increase blood glucose levels. They convert glycogen into glucose (this process is called glycogenolysis). The glucose is released into the bloodstream, increasing blood sugar levels. Hypoglycemia, the state of having low blood sugar, is treated by restoring the blood glucose level to normal by the ingestion or administration of dextrose or carbohydrate foods. It is often self-diagnosed and self-medicated orally by the ingestion of balanced meals. In more severe circumstances, it is treated by injection or infusion of glucagon.


When levels of blood sugar rise, whether as a result of glycogen conversion, or from digestion of a meal, a different hormone is released from beta cells found in the Islets of Langerhans in the pancreas. This hormone, insulin, causes the liver to convert more glucose into glycogen (this process is called glycogenesis), and to force about 2/3 of body cells (primarily muscle and fat tissue cells) to take up glucose from the blood through the GLUT4 transporter, thus decreasing blood sugar. When insulin binds to the receptors on the cell surface, vesicles containing the GLUT4 transporters come to the plasma membrane and fuse together by the process of exocytosis, thus enabling a facilitated diffusion of glucose into the cell. As soon as the glucose enters the cell, it is phosphorylated into Glucose-6-Phosphate in order to preserve the concentration gradient so glucose will continue to enter the cell.[1] Insulin also provides signals to several other body systems, and is the chief regulatory metabolic control in humans.

There are also several other causes for an increase in blood sugar levels. Among them are the 'stress' hormones such as epinephrine (also known as adrenaline), several of the steroids, infections, trauma, and of course, the ingestion of food.

Diabetes mellitus type 1 is caused by insufficient or non-existent production of insulin, while type 2 is primarily due to a decreased response to insulin in the tissues of the body (insulin resistance). Both types of diabetes, if untreated, result in too much glucose remaining in the blood (hyperglycemia) and many of the same complications. Also, too much insulin and/or exercise without enough corresponding food intake in diabetics can result in low blood sugar (hypoglycemia).

Hormones that influence blood glucose level

Hormone Tissue of Origin Metabolic Effect Effect on Blood Glucose
Insulin Pancreatic β Cells 1) Enhances entry of glucose into cells; 2) Enhances storage of glucose as glycogen, or conversion to fatty acids; 3) Enhances synthesis of fatty acids and proteins; 4) Suppresses breakdown of proteins into amino acids, of adipose tissue into free fatty acids. Lowers
Somatostatin Pancreatic δ Cells 1) Suppresses glucagon release from α cells (acts locally); 2) Suppresses release of Insulin, Pituitary tropic hormones, gastrin and secretin. Lowers
Glucagon Pancreatic α Cells 1) Enhances release of glucose from glycogen; 2) Enhances synthesis of glucose from amino acids or fatty acids. Raises
Epinephrine Adrenal medulla 1) Enhances release of glucose from glycogen; 2) Enhances release of fatty acids from adipose tissue. Raises
Cortisol Adrenal cortex 1) Enhances gluconeogenesis; 2) Antagonizes Insulin. Raises
ACTH Anterior pituitary 1) Enhances release of cortisol; 2) Enhances release of fatty acids from adipose tissue. Raises
Growth Hormone Anterior pituitary Antagonizes Insulin Raises
Thyroxine Thyroid 1) Enhances release of glucose from glycogen; 2) Enhances absorption of sugars from intestine Raises

Food and blood sugar regulation

Some edible mushrooms are noted for the ability to lower blood sugar levels including Reishi,[2][3] Maitake[4][5][6][7][8][9] Agaricus blazei [10][11][12][13] as well as some others.

Some minerals play roles in glucose regulation: see Chromium_in_glucose_metabolism for example.


  1. Ebey Soman, Scienceray, Regulation of Glucose by Insulin, May 4, 2009. Retrieved November 1, 2009.
  2. Zhang HN, Lin ZB (February 2004), "Hypoglycemic effect of Ganoderma lucidum polysaccharides", Acta Pharmacol. Sin., 25 (2): 191–5, PMID 14769208
  3. Yang BK, Jung YS, Song CH (November 2007), "Hypoglycemic effects of Ganoderma applanatum and Collybia confluens exo-polymers in streptozotocin-induced diabetic rats", Phytother Res, 21 (11): 1066–9, doi:10.1002/ptr.2214, PMID 17600864CS1 maint: multiple names: authors list (link)
  4. Konno S, Tortorelis DG, Fullerton SA, Samadi AA, Hettiarachchi J, Tazaki H. (Dec 2001), "A possible hypoglycaemic effect of maitake mushroom on Type 2 diabetic patients.", Diabet Med., 18 (12): 1010, doi:10.1046/j.1464-5491.2001.00532-5.x, PMID 11903406CS1 maint: multiple names: authors list (link)
  5. Hong L, Xun M, Wutong W. (Apr 2007), "Anti-diabetic effect of an alpha-glucan from fruit body of maitake (Grifola frondosa) on KK-Ay mice.", J Pharm Pharmacol, 59 (4): 575–82, doi:10.1211/jpp.59.4.0013, PMID 17430642CS1 maint: multiple names: authors list (link)
  6. Kubo K, Aoki H, Nanba H. (Aug 1994), "Anti-diabetic activity present in the fruit body of Grifola frondosa (Maitake). I.", Biol Pharm Bull., 17 (8): 1106–10, doi:10.1248/bpb.17.1106, PMID 7820117CS1 maint: multiple names: authors list (link)
  7. Lo HC, Hsu TH, Chen CY. (2008), "Submerged culture mycelium and broth of Grifola frondosa improve glycemic responses in diabetic rats.", Am J Chin Med., 36 (2): 265–85, doi:10.1142/S0192415X0800576X, PMID 18457360CS1 maint: multiple names: authors list (link)
  8. Manohar V, Talpur NA, Echard BW, Lieberman S, Preuss HG. (Jan 2002), "Effects of a water-soluble extract of maitake mushroom on circulating glucose/insulin concentrations in KK mice.", Diabetes Obes Metab., 4 (1): 43–8, doi:10.1046/j.1463-1326.2002.00180.x, PMID 11874441CS1 maint: multiple names: authors list (link)
  9. Horio H, Ohtsuru M. (Feb 2001), "Maitake (Grifola frondosa) improve glucose tolerance of experimental diabetic rats.", J Nutr Sci Vitaminol (Tokyo)., 47 (1): 57–63, doi:10.3177/jnsv.47.57, PMID 11349892
  10. Liu Y, Fukuwatari Y, Okumura K; et al. (June 2008), "Immunomodulating Activity of Agaricus brasiliensis KA21 in Mice and in Human Volunteers", Evidence-based Complementary and Alternative Medicine, 5 (2): 205–219, doi:10.1093/ecam/nem016, PMC 2396466, PMID 18604247. Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  11. Kim YW, Kim KH, Choi HJ, Lee DS (April 2005), "Anti-diabetic activity of beta-glucans and their enzymatically hydrolyzed oligosaccharides from Agaricus blazei", Biotechnol. Lett., 27 (7): 483–7, doi:10.1007/s10529-005-2225-8, PMID 15928854.CS1 maint: multiple names: authors list (link)
  12. Hsu CH, Liao YL, Lin SC, Hwang KC, Chou P. (January–February 2007), "The mushroom Agaricus Blazei Murill in combination with metformin and gliclazide improves insulin resistance in type 2 diabetes: a randomized, double-blinded, and placebo-controlled clinical trial.", J Altern Complement Med., 13 (1): 97–102, doi:10.1089/acm.2006.6054, PMID 17309383CS1 maint: multiple names: authors list (link) (Primary result, not review)
  13. Fortes RC, Novaes MR, Recôva VL, Melo AL. (January 2009), "Immunological, hematological, and glycemia effects of dietary supplementation with Agaricus sylvaticus on patients' colorectal cancer.", Exp Biol Med (Maywood)., 234 (1): 53–62, doi:10.3181/0806-RM-193, PMID 18997106CS1 maint: multiple names: authors list (link)


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