Hyperinsulinemia
| Hyperinsulinemia | |
|---|---|
| Classification and external resources | |
| ICD-9 | 251.6 |
Hyperinsulinemia, or hyperinsulinaemia is a condition which there are excess levels of insulin circulating in the blood than expected relative to the level of glucose. While it is often mistaken for diabetes or hyperglycaemia, hyperinsulinemia can result from a variety of metabolic diseases and conditions. While hyperinsulinemia is often seen in people with early stage type 2 diabetes mellitus, it is not the cause of the condition and is only one symptom of the disease. Type 2 diabetes only occurs when pancreatic beta-cell function is impaired. Hyperinsulinemia can be seen in a variety of conditions including diabetes mellitus type 2, in neonates and in drug induced hyperinsulinemia
Hyperinsulinemia is associated with hypertension, obesity, dyslipidemia, and glucose intolerance.[1] These conditions are collectively known as Metabolic syndrome.[2] This close association between hyperinsulinemia and conditions of metabolic syndrome suggest related or common mechanisms of pathogenicity.[1] Hyperinsulinemia has been shown to "play a role in obese hypertension by increasing renal sodium retention".[1] Insulin has a regulatory role in the transportation of cations across the cell membrane.[1] Elevated circulating insulin levels, such as in the case of hyperinsulinemia, cause intracellular sodium concentrations to increase, and intracellular potassium concentrations to decrease.[1] This alteration in cation concentrations both intracellularly and extracellularly contribute to hypertension.[1] Since hypertension is related to all other conditions of metabolic syndrome it can then be extrapolated that cation transport is ubiquitously associated with obesity, dyslipidemia, and glucose intolerance as well.[1] Furthermore, the alteration of cation transport across the membrane may serve as a marker for insulin resistance.[1]
In type 2 diabetes, the cells of the body become resistant to the effects of insulin as the receptors which bind to the hormone become less sensitive to insulin concentrations resulting in hyperinsulinemia and disturbances in insulin release.[3] With a reduced response to insulin, the beta cells of the pancreas secrete increasing amounts of insulin in response to the continued high blood glucose levels resulting in hyperinsulinemia. In insulin resistant tissues, a threshold concentration of insulin is reached causing the cells to uptake glucose and therefore decreases blood glucose levels. Studies have shown that the high levels of insulin resulting from insulin resistance might enhance insulin resistance.[3]
Studies on mice with genetically reduced circulating insulin suggest that hyperinsulinemia plays a causal role in high fat diet-induced obesity. In this study, mice with reduced insulin levels expended more energy and had fat cells that were reprogrammed to burn some energy as heat.[4]
Hyperinsulinemia in neonates can be the result of a variety of environmental and genetic factors. If the mother of the infant is a diabetic, and does not properly control her blood glucose levels, the hyperglycemic maternal blood can create a hyperglycemic environment in the fetus. To compensate for the increased blood glucose levels, fetal pancreatic beta cells can undergo hyperplasia. The rapid division of beta cells results in increased levels of insulin being secreted to compensate for the high blood glucose levels. Following birth, the hyperglycemic maternal blood is no longer accessible to the neonate resulting in a rapid drop in the newborn’s blood glucose levels. As insulin levels are still elevated this results in hyperinsulinemia. To treat the condition, high concentration doses of glucose are given to the neonate as required maintaining normal blood glucose levels. The hyperinsulinemia condition subsides after one to two days.[5]
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Causes[edit]
Since hyperinsulinemia and obesity are so closely linked it is hard to determine whether hyperinsulinemia causes obesity or obesity causes hyperinsulinemia, or both. Obese people have an excess of adipose tissue. Adipose tissue is known to secrete various metabolites, hormones and cytokines that may play a role in causing hyperinsulinemia.[6] Specifically cytokines secreted by adipose tissue directly effect the insulin signalling cascade, and thus insulin secretion.[7] Adiponectins are cytokines that are inversely related to percent body fat; that is people with a low body fat will have higher concentrations of adiponectins where as people with high body fat will have lower concentrations of adiponectins. Weyer "et al,." (2011) have discovered that hyperinsulinemia can be due in large part to low adiponectin concentrations in obese people.[7]
Effects[edit]
- May lead to hypoglycemia or diabetes
- Increased risk of PCOS
- Increased synthesis of VLDL (hypertriglyceridemia)
- Hypertension (insulin increases sodium retention by the renal tubules)
- Coronary Artery Disease (increased insulin damages endothelial cells)
- Increased risk of cardiovascular disease
- Weight gain and lethargy (possibly connected to an underactive thyroid)
Symptoms[edit]
There are often no visible symptoms of hyperinsulinemia unless hypoglycaemia (low blood sugar) is present.
Some patients may experience a variety of symptoms when hypoglycaemia is present, including:[9]
- Temporary muscle weakness
- Brain fog
- Fatigue
- Temporary thought disorder, or inability to concentrate
- Visual problems such as blurred vision or double vision
- Headaches
- Shaking/Trembling
- Thirst
If a person experiences any of these symptoms, a visit to a qualified medical practitioner is advised. Internet information does not substitute for advice by a medical professional, and diagnostic blood testing may be required.
Treatment[edit]
Treatment is typically achieved via diet and exercise, although Metformin may be used to reduce insulin levels in some patients (typically where obesity is present). A referral to a dietician is beneficial. Another method used to lower excessively high insulin levels is organic Cinnamon as was demonstrated when supplemented in clinical human trials.[10]
A low carbohydrate diet is particularly effective in reducing hyperinsulinism.
A healthy diet that is low in simple sugars and processed carbohydrates, and high in fiber, and vegetable protein is often recommended. This includes replacing white bread with whole-grain bread, reducing intake of foods composed primarily of starch such as potatoes, and increasing intake of legumes and green vegetables, particularly soy.[11]
Regular monitoring of weight, blood sugar, and insulin are advised, as hyperinsulinemia may develop into diabetes mellitus type 2.
It has been shown in many studies that physical exercise improves insulin sensitivity.[12] The mechanism of exercise on improving insulin sensitivity is not well understood however it is thought that exercise causes the glucose receptor GLUT4 to translocate to the membrane.[13] As more GLUT4 receptors are present on the membrane more glucose is taken up into cells decreasing blood glucose levels which then causes decreased insulin secretion and some alleviation of hyperinsulinemia.[12] Another proposed mechanism of improved insulin sensitivity by exercise is through AMPK activity.[12] The beneficial effect of exercise on hyperinsulinemia was shown in a study by Solomon "et al.," (2009) where they found that improving fitness through exercise significantly decreases blood insulin concentrations.[12]
Common misconceptions[edit]
- Hyperinsulinemia is often mistaken for diabetes or hypoglycaemia. These are separate, albeit related, conditions. Treatment may overlap for these conditions, but medical advice should always be sought.
See also[edit]
- Metabolic syndrome (Syndrome X)
- Acanthosis nigricans
References[edit]
- ^ a b c d e f g h Modan, Michaela; Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shitrit A, & Fuchs Z. (March 1985). "Hyperinsulinemia: A link between hypertension obesity and glucose intolerance". J. Clin. Invest. 75: 809–817.
- ^ Danker, Rache; Chetrit A, Shanik MH, Raz I, & Roth J (August 2009). "Basal-stat hyperinsulinemia in healthy normoglycemic adults is predictive of type 2 diabetes over a 24-year follow-up". Diabetes Care 32 (8): 1464–1466.
- ^ a b Shanik, M.H., Yuping, X., Skrha, J., Danker, R., Zick, Y., and Roth, J. (2008) Insulin Resistance and Hyperinsulinemia “Diabetes Care”, 31(2):s262-s268. Doi 10.2337/dco8-s264
- ^ Mehran, Arya E.; Nicole M. Templeman, G. Stefano Brigidi, Gareth E. Lim, Kwan-Yi Chu, Xiaoke Hu, Jose Diego Botezelli, Ali Asadi, Bradford G. Hoffman, Timothy J. Kieffer, Shernaz X. Bamji, Susanne M. Clee, James D. Johnson (6). "Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production". Cell Metabolism 16 (5): 723–737.
- ^ Ferry, R.J. (2010). Hyperinsulinism “Medscape”.
- ^ Matsuzawa, Y; Fanahashi T, & Nakamura T (1999). "Moleculare mechanism of metabolic syndrome X: contribution of adiposcyte-derived bioactive substances.". Ann NY Acad Sci 892: 146–154.
- ^ a b Weyer, C; Funahachi T, Tanaka S, Hotta K, Matsuzawa Y, Pratley RE, & Tataranni PA (2011). "Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia". The Journal of Clinical Endocrinology & Metabolism 86 (5): 1930–1935.
- ^ [1], Dieting and exercise
- ^ Hyperinsulinemia
- ^ http://onlinelibrary.wiley.com/doi/10.1111/j.1463-1326.2006.00694.x/abstract
- ^ American Journal of Clinical Nutrition, Vol. 87, No. 1, 162-167, January 2008. www.ajcn.org/content/87/1/162.abstract?ijkey=3a106187f1678d56840e6dab576a51489985c84d&keytype2=tf_ipsecsha
- ^ a b c d Solomon, Thomas P; Haus JM, Kelly KR, Cook MD, Riccardi M, Rocco M, Kashyap SR, Barkowkis H, & Kirwan JP (2009). "Randomized trial on the effects of a 7-d low-glycemic diet and exercise intervention on insulin resistance in older obese humans". Am J Clin Nutr 90: 1222–1229.
- ^ Lund, S; Holman GD, Schmitz O, & Pedersen O (1995). "Contraction stimulates translocation of glucose transporter GLUT4 in skeletal muscle through a mechanism distinct from that of insulin.". Proc. Natl. Acad. Sci 92 (13): 5817–5821.
