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”.
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”.
Chronically elevated levels of circulating blood glucose has damaging effects throughout our body through the formation of advanced glycated end products (“AGE’s”). These “AGEs” cause organ damage, resulting in the development of conditions such as diabetic nephropathy (kidney damage), diabetic neuropathy (nerve damage), diabetic retinopathy (eye damage) and cardiovascular disease (damage to the heart and blood vessels). It is therefore essential to clear the bloodstream of excess circulating glucose to maintain normal levels. However, excess glucose levels within our cells also has damaging effects. As an adaptive response to chronic excessive carbohydrate consumption, our bodies downregulate the number of insulin receptors as well as the sensitivity to insulin binding. This results in the development of insulin resistance. To overcome this adaptive cellular response, our body needs to produce more insulin to clear glucose from the bloodstream. Eventually, we cannot make adequate insulin and blood glucose levels start to rise, leading to the development of impaired glucose tolerance and type 2 diabetes. Insulin resistance, impaired glucose tolerance and diabetes are not the result of caloric excess. The conditions of carbohydrate intolerance that develop as a result of chronic excessive carbohydrate consumption. While insulin is essential for survival, elevated levels of insulin are associated with inflammation, increased cancer risk and increased atherosclerosis (leading to the development of cardiovascular disease). 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 <4.5mmol/L = insulin sensitive, while a score of >5.5mmol/L = early insulin resistance. Insulin resistance is formally diagnosed when HbA1c is 5.7-6.4mmol/L whereas diabetes is diagnosed when HbA1c is >6.5mmol/L.
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
