insulin resistance weight gain

Insulin resistance and weight gain: chicken or egg?

Whilst there is a definite relationship between insulin resistance and weight gain, which one comes first remains unclear. Both insulin resistance and weight gain are risk factors for type 2 diabetes and many other chronic diseases. Let’s examine their relationship.

Recall of definitions

Let’s begin with a brief recall of key definitions: insulin facilitates sugar (glucose) to move into the cells to be used and also for fat to be stored.

Insulin resistance is when a groups of cells becoming increasingly resistant to the effects of insulin. The impact of insulin resistance depends on its specific role at that group of cells: there is reduced transport of glucose into muscle cells, fat is broken down into smaller components, called free fatty acids and the liver continues to make new glucose and fat. In case you missed it check out Introduction to insulin, insulin resistance and type 2 diabetes to find out more.

A vicious cycle?

Insulin resistance and weight gain exacerbate one another. Factors that either contribute to gaining weight or are characteristic of excess weight gain, such as excess body fat, visceral fat (fat around the organs), poor diet and low physical activity, contribute to insulin resistance. Additionally, insulin resistance is associated with high levels of insulin and insulin promotes the storage of fat.

Both genetic and lifestyle factors determine how insulin sensitive (or insulin resistant) someone is and their weight status. Simple changes to diet and exercise, whilst creating a negative energy balance, effectively improve insulin sensitivity and result in weight loss. Check out some of the specific factors below.

Weight gain factors → insulin resistance

Excess body fat

Excess body fat and being overweight is the greatest risk factor for insulin resistance: over one third of overweight individuals are insulin resistant and the combination of insulin resistance and excess body fat is associated with a host of chronic diseases (1). Fat cells secrete a range of substances, such as free fatty acids, hormones and proinflammatory substances. These substances can cause insulin resistance. As the size of fat cells increases, the volume of all the substances secreted increases and the degree of insulin resistance increases (2).

Fat stores can grow by either increasing in size (hypertrophy), or number (hyperplasia). The number of fat cells someone can make is finite and therefore at that specific point, if someone is in a positive energy balance, their fat cells must grow by hypertrophy. The hypertrophy of fat cells can have damaging effects and increase secretion of substances that subsequently result in insulin resistance (2).

This supports the personal fat threshold concept, whereby every individual has a different tolerance of fat, and when they reach this and go over it, it results in ill health, such as type 2 diabetes (3). However, you can be insulin resistant and have type 2 diabetes without being overweight.

Intra-abdominal body fat

As well as the amount of body fat contributing to insulin resistance, its location on the body also contributes to insulin resistance. Central body fat around the abdomen, which can be measured from the waist-to-hip ratio is associated with insulin resistance, type 2 diabetes and cardiovascular disease (4). This is due to the specific type of fat that is stored there called visceral fat which covers the organs – unlike subcutaneous fat that is stored just under the skin.

Visceral fat is strongly associated with insulin resistance, is particularly active and readily secretes harmful substances. These harmful substances can then promote insulin resistance in the organs that they are in close proximity to (4).

Also, someone may not appear to be overweight, but can still have a high proportion of visceral fat –sometimes referred to as ‘skinny fat’ or ‘metabolically unhealthy non-obese’. Key characteristics of the metabolically unhealthy non-obese individual includes, poor glucose tolerance, markers of insulin resistance and inflammation and likelihood to develop type 2 diabetes and cardiovascular disease (5). Assessing our clients body composition accurately is something we do at the clinic as part of our sessions. This allows us to identify one’s visceral fat, fat mass, muscle mass, water levels and so forth.

Diet

Weight gain is due to an overall positive energy balance which can be due to consuming a diet in an energy surplus. A continual excess of energy become a stress to the body and the cells send stress signals (reactive oxygen species) to communicate this situation to the rest of the body. These stress signals cause insulin resistance (6).

Similarly, to the body’s own fat stores secreting harmful substances which contribute to insulin resistance, this occurs from certain foods. In particular, foods that are high in sugars, processed and refined (carbohydrates and fats – specifically trans fats) and that have been heated at high temperatures contribute to insulin resistance (7).

Physical activity

Physical activity levels and exercise also affect the overall energy balance. Being overweight and being relatively inactive are insulin resistant states (8). Additionally, being overweight is associated with lower levels of physical activity (9,1).

It has been shown that individuals who are particularly overweight have significantly less capacity for glucose uptake than individuals who are lean, leading to insulin resistance and type 2 diabetes (10).

Physical activity and exercise enhance insulin sensitivity independent of weight loss – through enhancing glucose uptake into the muscles both with and without insulin and through increasing blood flood to the muscles and causing the growth of new healthy cells and subsequent muscle mass (11).

Insulin resistance → weight gain

Insulin is high and insulin is a fat-storage hormone

An insulin resistant state means that glucose is not able to get into the muscle cells effectively so the body responds by producing more insulin to try to help to get its job done. As a result, insulin resistance is associated with increased levels of insulin and one of the key roles of insulin is to make and store fat and prevent the breakdown of fat. Hence, the effects of high levels of insulin and insulin resistance results may be weight gain. Also, the process of new fat being made from carbohydrate stores is also increased in people with insulin resistance (12).

Take away messages

Insulin resistance and weight gain are strongly associated with one another

It’s highly likely that as one increases the other increases. Both of them have the same contributing factors and also contribute to one another. Both insulin resistance and excess weight are risk factors for chronic diseases, including type 2 diabetes. Taking a step to tackle either one of them will inevitably improve both!

Insulin resistance and propensity to gain weight varies between individuals

However, the tools of diet, physical activity and weight management are available to every individual and although they can’t change your genes, they can change the expression of your genes! If you feel as though you have hit a barrier with any one of these tools or understandably find them challenging, take a pause to work out what might best help you go forward. Forget about what hasn’t worked for you in the past. The right way forward is waiting for you! What could help you most to unlock that new healthy habit?

Insulin resistance and weight management are adaptable

By introducing small daily habits which improve your diet, physical activity and exercise levels. What step can you take today? Check out Improve insulin sensitivity with these exercise tips and 10 tips to improve insulin sensitivity – start implementing a few of these and you will be well on your way!

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References

  1. Viner et al. (2005). Prevalence of the insulin resistance syndrome in obesity.
  2. Kahn et al. (2010). Obesity and insulin resistance.
  3. Taylor et al. (2015). Normal weight individuals who develop type 2 diabetes: the personal fat threshold.
  4. Eckel et al. (2011). Obesity and type 2 diabetes: what can be unified and what needs to be individualised?
  5. Rhee et al. (2013). Metabolic health is more closely associated with coronary artery calcification than obesity.
  6. Fung et al. (2016). Hyperinsulinemia and Insulin resistance: scope of the problem
  7. Cordain et al. (2005). Origins and evolution of the western diet: health implications for the 21st century.
  8. DeFronzo (2009). From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus.
  9. Riebe et al. (2009). The relationship between obesity, physical activity and physical function in older adults.
  10. Gaster et al. (2001). GLUT4 is reduced in slow muscle fibres of type 2 diabetic patients: is insulin resistance in type 2 diabetes a slow, type 1 fibre disease?
  11. Colberg et al. (2010). Exercise and type 2 diabetes: the American college of sports medicine and the American diabetes association: joint position statement.
  12. Sanders et al. (2015). De novo lipogenesis in the liver in health and disease: more than just a shunting yard for glucose.
  13. Shanik et al. (2008). Insulin resistance and hyperinsulinemia. Is hyperinsulinemia the cart or the horse?