While overweight conditions and obesity are health concerns on their own, increased body weight and related increase in body fat, and here in particular organ fat, is also a risk factor for the development of insulin resistance and related metabolic diseases.
In conditions of reduced insulin sensitivity, the body does not properly respond to the effects of insulin, especially by the liver, muscle and fat (adipose) tissues. In order to help glucose to enter muscle and fat cells, the body compensates for the reduced insulin sensitivity by producing additional amounts of insulin. The result is an exceedingly high level of insulin in the blood and an over-stimulation of insulin-sensitive tissues until the body develops an insulin resistance or type-2 diabetes mellitus. Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG) are resulting intermediate conditions in the transition between normality and diabetes. People with impaired glucose metabolism are at high risk of progressing to type 2 diabetes. Therefore, it is commonly referred to as prediabetes.
Whereas early stages of type 2 diabetes mellitus are treated with oral medication or lifestyle intervention including dietary advice, insulin supplementation may eventually become necessary when pancreatic beta cells exhaust and lose the ability to produce insulin.
Considering the central role of insulin in metabolic control, insulin resistance is also the precursor of a cluster of associated diseases including obesity, type 2 diabetes, cardiovascular disease, and hypertension. This cluster is called the metabolic syndrome, and is also referred to as syndrome X, or insulin resistance syndrome (see figure below.)
Reducing body weight and fat at early stage helps to improve insulin sensitivity and stop further progression into diabetes. Therefore, weight loss strategies with diet and physical activity are usually important cornerstones in the first line of treatment of reduced insulin sensitivity and insulin resistance.
Existing research suggest that sugars replacement for isomaltulose can lower body fat production, in this case liver fat, with resulting positive effects on insulin sensitivity. In comparison to sucrose, Keyhani-Nejad et al (2015) observed that isomaltulose feeding for 22 weeks prevented non-alcoholic fatty liver and improved glucose tolerance in rats. The researchers further demonstrated that the different incretin response, along with the low effect of isomaltulose on GIP release in the early parts of the small intestine, plays a key role in the underlying mechanism. This emphasizes the potential of isomaltulose as a nutritional strategy to prevent fatty liver and insulin resistance independent of obesity. The physiological relevance of GIP for metabolic health and disease and related benefits of a low GIP release with isomaltulose have been described by the same researchers in a review (Pfeiffer and Keyhani-Nejad 2018).