Researchers have found that a high-fat diet increases the metabolism of fructose in the small intestine, resulting in a fructose-specific metabolite known as glycerate being released into the circulation. The circulating glycerate can then cause damage to the pancreatic beta cells that produce insulin, increasing the risk of glucose tolerance diseases such as type 2 diabetes.
Although type 2 diabetes is generally found in older individuals, it is increasingly common in younger individuals. In the past 20 years alone, the prevalence of type 2 diabetes has doubled. Equally worrisome are the health risks associated with type 2 diabetes, including stroke and heart disease.
In type 2 diabetes, there are insufficient levels of insulin, a hormone that controls the flow of glucose to peripheral cells. This usually happens because of insulin resistance, which is when peripheral tissues don’t have a normal response to insulin and take up less glucose. The pancreas works overtime to secrete more insulin to compensate and eventually loses this ability. This results in an unhealthy build-up of glucose in the blood.
Many studies have been done on the influence of high-fat and fructose diets on the development of type 2 diabetes. Previous studies have shown that fructose causes harmful effects in the liver. However, other research has found that these effects are mostly prevented by the metabolism of fructose in the small intestine; the liver only participates in the metabolic process if the fructose content is too high.
These observations prompted the researchers to investigate the metabolism of fructose in the small intestine to determine its role in the development of type 2 diabetes. Experiments in mice consuming a high-fat diet, along with corresponding amounts of sugar, led to a higher metabolism of fructose in the small intestine. This increased production of glycerate in the small intestine was then released and circulated in the blood. This indicates that the metabolism of fructose in the small intestine is increased by a high-fat diet that increases the production of circulating glycerate.
More evidence for glycerate’s role in diabetes was uncovered when the researchers looked at data from patients with abnormally high levels of circulating glycerate who have a disease known as D-glycerate aciduria. The analysis found that this abnormality was an independent and significant risk factor for diabetes for these individuals. More tests were performed to evaluate the impact of circulating glycerate- and fructose-fed mice on normal and high-fat diet mice.
The results suggested that the glucose disturbances seen in the mice injected with glycerate were due to a reduction in circulating insulin, as opposed to insulin resistance. Histological analysis confirmed reduced numbers and increased death of the beta cells that produce insulin in the regions of the pancreatic islet in the mice injected with glycerate, leading to decreased insulin levels.
The study results collectively indicate that long-term exposure to high glycerate levels due to excessive consumption of dietary fat and high fructose diets increases the risk of pancreatic islet cell damage and diabetes.
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