Insulin Resistance: What is it, and can it be cured?

20 Feb 2014

First of all, what is insulin?

 

Insulin is a polypeptide hormone that is released from the Beta cells within the Pancreas when blood-glucose levels are high (hyperglycaemia). The key cells that insulin acts upon are liver, muscle and adipose tissue and will:

 

  • Transfer of glucose into cells.

  • Increases the rate at which glucose is converted into glycogen (glycogenesis).

  • Increases the uptake of amino acids (building blocks of protein) into cells and increases protein synthesis.

  • Increases the rate of glucose converted into fatty acids (lipogenesis).

  • Slows the formation of glucose from lactic acid and amino acids (glyconeogenesis).

  • Slows the conversion of glycogen into glucose (glycogenolysis).

 

Insulin can also be secreted following consumption of the amino acids called arginine and leucine, as well as a hormone known as glucose-dependant insulinotropic peptide (GIP) which is released from the small intestine in response to the presence of glucose in the gastrointestinal tract. Digestion and absorption of foods containing carbohydrates and/or proteins, therefore, will provide a great stimulus for the release of insulin (Tortora and Derrickson, 2011).

 

Growth hormone and andrenocorticotropic hormone can also induce insulin secretion indirectly as these act to elevate blood glucose.

 

A lack of insulin can cause a build up of glucose in the blood, causing blood-glucose concentrations to become that high, the kidneys become overwhelmed and glucose is lost in the urine, taking large volumes of water with it. This is known as Diabetes Mellitus. Type 1 diabetes is when this condition is caused due to the body’s failure to produce insulin, whereas Type 2 diabetes is caused by the body’s cells failing to use insulin correctly (Powers and Howley, 2012).

 

The latter, is also known as and or associated with insulin resistance, and will be the main topic featured in this article.

 

Insulin Resistance

 

Insulin resistance is a condition in which normal insulin levels have a below normal response and is associated with obesity, non-insulin dependant diabetes mellitus, high blood pressure and coronary heart disease (Ashraff, Sidiqui and Carline, 2013). The most common factor associated with insulin resistance is an excessive fat mass, mainly that located in the abdominal region (O’Rahilly, 1997; Abate, et al., 1995; Goodpaster, et al., 1997). Other symptoms include:

 

  • Depression (Hannon, et al., 2013).

  • Asthma-like symptoms (Theusen, et al., 2009)

  • Hot flashes (Thurston, et al., 2012)

  • Skin tags (Sudy, et al., 2008)

  • Sleep complaints (Pyykonen, et al., 2012; Suarez, 2008)

  • Excessive daytime sleepiness (Liu, Kushida and Reaven, 2013)

  • Reduced cognitive ability and dementia symptoms (Cholerton, Baker and Craft, 2013).

 

The main causes of inslin resistance appear to be lack of exercise, excessively high caloric diet particularly dominant in carbohydrates, and chronic unstable blood-glucose concentrations caused by frequent consumption of simple carbohydrates throughout the day. This coincides with a typical modern westerner’s diet, example given below:

 

  • Breakfast: Cereal, Toast, Fruit Juice

  • Mid-morning snack: Crisps, chocolate bar, cereal bar, soft-drinks, sugar in tea/coffee, fruit

  • Lunch: Sandwich, pasta with sauce, wraps, soft-drinks, fruit,

  • Afternoon snack: Crisps, chocolate, sweets, energy drinks, soft drinks, sugar in tea/coffee, fruit

  • Dinner: Pasta, bread, takeaway

  • Desert: Ice cream, cake, chocolate, jelly, fruit.

 

As discussed earlier, the resulting increase in blood-glucose concentration following consumption of carbohydrate provides a strong stimulus for the secretion of insulin. Consuming the foods listed above will produce what can be seen as a cyclic effect on blood-glucose/insulin in that a sudden spike in blood-glucose will be followed soon after by a crash in energy levels. Subsequently, the common pattern is then for the individual to seek more carbohydrates in order to quickly re-establish glucose levels, and thus induces a never-ending cycle. This up-and-down affect will ultimately place fatigue on the cellular mechanisms responsible for the signalling of insulin and subsequent transfer of glucose across the cell membrane. In time, insulin resistance and even type 2 diabetes can occur.

 

Treatment

 

Reviewing the symptoms and mechanisms above, it doesn’t take a “rocket-scientist” to guess a number of potentially successful interventions in the treatments of insulin resistance and/or type 2 diabetes.

 

Despite most believing that a diet high in complex carbohydrates and low in fat is deemed healthy, diets that are higher in fat and protein are becoming more of a popular recommendation amongst “experts” (Atkins, 2002). This would make sense as the frequent consumption of carbohydrates and its association with fat gain appears to be a significant predictor of insulin resistance.

 

Individuals with symptoms of insulin resistance are therefore advised to consume a diet that is dominant in quality fats and proteins. An example of good fats are listed below:

 

  • Coconut oil

  • Kerry gold butter

  • Olive oil (raw/cold)

  • NutsSeeds

  • Avocado

  • Meat

  • Oily fish

  • Eggs

 

Of course, not all carbohydrates are created equal, and it is certainly advised that trained individuals consume suffience carbohydrates from those rich in nutrients and fibre, however, It is recommended that food items labelled “low-fat” should be avoided as these typically contain large quantities of simple carbohydrates or sugars (Astrup, et al., 2000).

 

Insulin sensitivity has been found to improve following a resistance training programme (Cryomans, et al., 2013) and significantly increases when resistance training is performed simultaneously to a high-fat diet (Farias, et al., 2012).

 

Author: Karl Page

 

References

 

Abate, N., Garg, A., Peshock, R. M., Stray-Gundersen, J. and Grundy, S. M., 1995. Relationships of generalized and regional adiposity to insulin sensitivity in men. Journal of Clinical Investigation. 96(1), pp. 88-98.

 

Ashraff, S., Siddiqui, M. A. and Carline, T. E., 2013. Obesity and Insulin Resistance: Management in Diabetes. Turkish Journal of Endocrinology & Metabolism. 17(3), pp. 57-62.

 

Astrup, A., Ryan, L., Grunwald, G. K., Storgaard, M., Saris, W., Melanson, E. and Hill, J. O., 2000. The role of dietary fat in body fatness: evidence from a preliminary meta-analysis of ad libitum low-fat dietary intervention studies. British Journal of Nutrition. 83(1), pp. 25-32.

 

Atkins, R. C., 2002. Dr Atkins’ new diet revolution. New York: Avon Books. Cholerton, B., Baker, L. D. and Craft, S., 2013. Insulin, cognition and dementia. European Journal of Pharmacology. 719(1-3), pp. 170-179.

 

Cryomans, D. M., Paparisto, E., Lee, M. M., Brandt, N., Le, B. K., Lohan, D., Lee, C. C. and Roberts, C. K., 2013. Resistance training improves indices of muscle insulin sensitivity and B-cell function in overweight/obese, sedentary young men. Journal of Applied Physiology. 115(9), pp. 1245-1249.

 

Farias, J. M., Maggi, R. M., Tromm, C. B., Silva, L. A., Luciano, T. F., Marques, S. O., Lira, F. S., De Souza, C. T. and Pinho, R. A., 2012. Exercise training performed simultaneously to a high-fat diet reduces the degree of insulin resistance and improves adipR1-2/APPL1 protein levels in mice. Lipids in Health and Diseases. 11(1), pp. 134-142.

 

Goodpaster, B. H., Thaete, F, L., Simoneau, J. A. and Kelley, D. E., 1997. Subcutaneous Abdominal Fat and Thigh Muscle Composition Predict Insulin Sensitivity Independently of Visceral Fat. Diabetes. 46(10), pp. 1579-1585.

 

Hannon, T. S., Rofey, D. L., Lee, S. and Arslanian, A. A., 2013. Depressive symptoms and metabolic markers of risk for type 2 diabetes in obese adolescents. Pediatric Diabetes. 14(7), pp. 497-503.

 

Liu, A., Kushida, C. A. and Reaven, G. M., 2013. Risk for obstructive sleep apnea in obese, nondiabetic adults varies with insulin resistance status. Sleep & Breathing. 17(1), pp. 333-338. O’Rahilly, S. Science, medicine, and the future. Non-insulin dependant diabetes mellitus: the gathering storm. British Medical Journal. 314(7085), pp. 955-959.

 

Powers, S. K. and Howley, E. T., 2012. Exercise Physiology: Theory and Application to Fitness and Performance. 8th ed. New York: McGraw-Hill.

 

Pyykonen, A. J., Isomaa, B., Pesonen, A. K., Eriksson, J. G., Groop, L., Tuomi, T. and Raikkonen, K., 2012. Subjective sleep complaints are associated with insulin resistance in individuals without diabetes: The PPP-Botina Study. Diabetes Care. 35(11), pp. 2271-2278.

 

Suarez, E. C., 2008. Self-reported symptoms of sleep disturbance and inflammation, coagulation, insulin resistance and psychosocial distress: Evidence for gender disparity. Brain, Behaviour & Immunity. 22(6), pp. 960-968.

 

Sudy, E., Urbina, F., Maliqueo, M, and Sir, T., 2008. Screening of glucose/insulin metabolic alterations in men with multiple skin tags on the neck. Journal of the German Society of Dermatology. 6(10), pp. 852-855.

 

Thuesen, B. H., Husemoen, L. L. N., Hersoug, L. G., Pisinger, C. and Linneberg, A., 2009. Insulin resistance as a predictor of incident asthma-like symptoms in adults. Clinical & Experimental Allergy. 39(5), pp. 700-707.

 

Thurston, R. C., El Khoudary, S. R., Sutton-Tyrrell, K., Crandall, C. J., Strenfeld, B., Joffe, H., Gold, E. B., Selzer, F. and Matthews, K. A. 2012. Vasomotor symptoms and insulin resistance in the study of women’s health across the nation. The Journal of Clinical Endocrinology and Metabolism. 97(10), pp. 3487-3494.

 

Tortora, G. J. and Derrickson, B., 2011. Principles of anatomy and physiology, vol.1: Organisation, support and movement, and control systems of the human body. 13th ed. Hoboken, N.J: Wiley.

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