Glucose Homeostasis & Insulin Resistance

 
 

When we consume any form of carbohydrate, our glucose (sugar) levels rise. When glucose levels rise, this triggers the release of a hormone (chemical messenger) called insulin. Glucose can move freely into some cells; however, other cells such as fat cells and muscle cells need insulin to unlock the transporters (gates) that allow glucose to enter these cells. Once inside our cells, glucose is used immediately as energy, converted to glycogen for later use through a process called “glycogenesis”, or converted to triglycerides for storage through a process called “lipogenesis”.  

Glucose Homeostasis and insulin Resistance.png

When glucose and insulin levels fall, we release another hormone called glucagon, which enables us to convert glycogen (stored glucose) back to glucose. Our stored fats (triglycerides) can only be accessed when insulin levels are low because insulin inhibits hormone-sensitive lipase, which is required to break down triglycerides via a process called “lipolysis”.

insulin-blood-sugar-monitoring

Chronically elevated levels of circulating blood glucose levels results in the formation of advanced glycated end products (“AGE’s”), which cause organ damage, such as diabetic nephropathy (kidney damage), neuropathy (nerve damage), retinopathy (eye damage) and cardiovascular disease (damage to the heart and blood vessels). It is therefore essential to clear the bloodstream of glucose to maintain normal levels. However, excess glucose is also toxic to our cells. As an adaptive response to chronic excessive carbohydrate consumption, insulin sensitivity is lost. This occurs via the down regulation of the insulin pathway and a reduction in the number of transporters/gates that allow glucose to enter the cells. To overcome this adaptive cellular response, our body needs to produce more and more insulin levels to clear glucose from the blood stream. Eventually, we are not able to make adequate insulin and blood glucose levels start to rise, leading to the development of impaired glucose tolerance, which can progress into type 2 diabetes. So insulin resistance, impaired glucose tolerance and diabetes are not the result of caloric excess. They are the result of chronic excessive carbohydrate consumption. Insulin is essential for survival; however at higher levels, insulin has pro-inflammatory, pro-cancer, pro-atherogenic effects which further increase our risk of developing lifestyle-related health conditions. Please refer to the Society of Metabolic Health for Practitioners for more information on insulin resistance, which is available at  https://thesmhp.org/

What are the indicators of insulin resistance?

  • Waist circumference greater than 94cm in men and 80cm in women

  • Waist to hip ratio of greater than 0.86 in women and >0.95 in men

  • Clinical signs such as skin tags, acanthosis nigricans

HOMA-IR stands for Homeostatic Model Assessment of Insulin Resistance. It's a mathematical model used to estimate insulin resistance. HOMA-IR is calculated using fasting blood glucose and fasting insulin levels.  Several studies suggest that a score of >2 is indicative of insulin resistance. "Normal" values appear to vary greatly by population, however an optimal score is usually < 1 and a score between 1.1-1.9 indicates there may be some insulin resistance.

We can assess for damage done to red blood cells (RBC’s) by glucose by measuring HbA1c, which is a measure of the amount of RBC glycation. A score of <4.56mmol/mol = insulin sensitive and anything >5.5 6mmol/mol = early insulin resistance. Insulin resistance is formally diagnosed when HbA1c is 5.7-6.46mmol/mol where as diabetes is diagnosed when HbA1c is >6.6mmol/mol.

For further information on insulin resistance, please refer to the below linked handout on insulin resistance on the Society of Metabolic Health for Practitioners website under the tools and handout tab

https://thesmhp.org/wp-content/uploads/2024/08/insulin-resistance-v5.pdf

 
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