Introduction[edit | edit source]
Insulin, a hormone produced by the beta cells in the pancreas, is normally released in small amounts after each meal to help transport glucose into the body’s cells, where it is needed for energy production. Insulin resistance (IR) refers is to an impaired biologic response to insulin stimulation of target tissues, essentially the liver, muscle, and adipose tissue. In IR alterations occur in the signalling pathways that modulate glucose uptake into cells, especially skeletal muscle cells, resulting in impaired glucose homeostasis and hyperinsulinemia.
Metabolic Effects[edit | edit source]
The metabolic effect of insulin resistance may cause hyperglycemia, hypertension, dyslipidemia, visceral adiposity, hyperuricemia, elevated inflammatory markers, endothelial dysfunction (inflammatory changes eg atherosclerosis), and a prothrombic state (increased risk of blood clot).
- Hyperinsulinaemia and IR can affect the proportion of the body’s lipids, notably increasing the amount of triglycerides and small dense lipoproteins in the blood and decreasing the amount of high density lipoproteins, the “good cholesterol”.
- IR may cause increased sodium retention (a risk factors for hypertension). Essential hypertension is present in roughly 50% of people who have insulin resistance.
IR has been associated with many chronic health conditions for example: cardiovascular disease, hypertension, metabolic syndrome, polycystic ovarian syndrome, type 2 diabetes, obesity, and nonalcoholic fatty liver disease. 
Etiology[edit | edit source]
Insulin resistance has complex metabolic traits and is a key risk factors for the development of chronic disease, as shown above. IR result from the interaction of environmental and genetic factors but the full extent of the genetic background to these conditions still needs research. Large-scale genome-wide association studies have helped advance the identification of common genetic variation associated with insulin resistance. However people who have IR have it as an acquired condition resulting from:
- Excess dysfunctional adipose tissue
- Physical inactivity
- Nutritional imbalance
- Medications ( eg glucocorticoids, anti-adrenergic, protease inhibitors, atypical antipsychotics, and some exogenous insulin)
- Increased sodium diets
- Glucose toxicity
- Lipotoxicity from excess circulating free fatty acids.
Management[edit | edit source]
Lifestyle intervention should be the first strategy for patients with IR syndrome. Physiotherapists can be involved in this important process.
- Increase exercise amounts: Exercise may be one way to improve insulin sensitivity. Notable improvements in insulin sensitivity are mainly driven by weight reduction. However when adaptations following weight loss are compared between weight loss and exercise, improvements in IR are greater from exercise-induced weight loss. Also, exercise-induced weight loss stimulates mitochondrial oxidative capacity and impacts endogenous glucose production by significantly suppressing unnecessary gluconeogenesis (see Exercise Physiology). The better results seen in exercise/weight loss combination may be influenced by exercise intensity, as it relates to changes in body composition. Dietary weight loss effectively lowers adipose tissue considerably, but does not influence muscle metabolism similar to exercise training. When both interventions are used together they are a powerful management tool in the management of IR.
- Getting more sleep may also improve insulin sensitivity.
- Dietician input re sodium reduction, fat reduction, calorie restriction, and attention to the glycemic index of foods.
- Pharmacist to educate the patient on the importance of medication compliance. For example taking medications to lower blood pressure, lipids, and diabetes. Also to encourage the patient to stop smoking and limit alcohol use, risk factors for insulin resistance.
References[edit | edit source]
- Freeman AM, Pennings N. Insulin resistance. InStatPearls [Internet] 2022 Jul 4. StatPearls Publishing. Available:https://www.ncbi.nlm.nih.gov/books/NBK507839/ (accessed 20.8.2022)
- Whillier S. Exercise and insulin resistance. Physical Exercise for Human Health. 2020:137-50. Available:https://pubmed.ncbi.nlm.nih.gov/32342455/ (accessed 20.8.2022)
- Pathology tests Insulin resistance Available:https://pathologytestsexplained.org.au/learning/index-of-conditions/insulin-resistance (accessed 20.8.2022)
- Mayo Clinic Metabolic Syndrome Available:https://www.mayoclinic.org/diseases-conditions/metabolic-syndrome/symptoms-causes/syc-20351916 (accessed 21.8.2022)
- Brown AE, Walker M. Genetics of insulin resistance and the metabolic syndrome. Current cardiology reports. 2016 Aug;18(8):1-8. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4911377/(accessed 21.8.2022)
- Keshel TE, Coker RH. Exercise training and insulin resistance: a current review. Journal of obesity & weight loss therapy. 2015 Jul;5(0 5). Available:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625541/ (accessed 21.8.2022)