All Sugars Are Not Alike: Isomaltulose Better Than Table Sugar for People with Type 2 Diabetes

► Table sugar (© Till Budde/DIfE)

German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE)

A press release of the Leibniz Association

15.2.2016

All Sugars Are Not Alike: Isomaltulose Better Than Table Sugar for People with Type 2 Diabetes

Potsdam-Rehbruecke – Like sucrose (table sugar), the natural disaccharide isomaltulose (PalatinoseTM) consists of glucose and fructose, but it is apparently more suitable for people with type 2 diabetes with regard to regulating blood glucose levels. This has now been confirmed in a new study carried out by the German Institute of Human Nutrition (DIfE), a partner in the German Center for Diabetes Research (DZD). The study showed for the first time on subjects with type 2 diabetes that the favorable metabolic effect of isomaltulose is due to the almost opposing release profiles of the gut hormones GLP-1 and GIP*.

The research team led by Farnaz Keyhani-Nejad and Andreas F. H. Pfeiffer of DIfE has now published its results in the journal Diabetes Care (Keyhani-Nejad et al. 2016; 39:e1-e2; DOI: 10.2337/dc15-1891).

Following isomaltulose ingestion, the rise in the blood glucose concentration is lower than after the intake of table sugar, although both types of sugar are composed of the same simple sugars and are completely digested and absorbed in the small intestine. This has been confirmed in various studies, but the metabolic mechanisms underlying this observation have been less explored. For this reason, the DIfE researchers investigated the effect of 50 g isomaltulose and 50 g sucrose in a crossover study of 10 adults with type 2 diabetes.

In the current study which compared isomaltulose with table sugar, the mean peak blood glucose concentrations after isomaltulose ingestion were 20 percent lower. Insulin secretion was even 55 percent lower. Likewise, the GIP concentration in blood increased only a little and reached its peak value only after 60 minutes. After intake of table sugar, however, GIP levels rose already after 15 minutes by more than double and then dropped sharply after about 60 minutes. With regard to GLP-1 secretion the scientists also observed differences between the two sugars. After ingestion of isomaltulose the GLP-1 levels rose in the test subjects faster and were sustained longer than following the intake of table sugar. With regard to glucagon secretion, the scientists found no significant differences.

The scientists assume that the different metabolic effects of the two disaccharides, which are composed of one molecule of glucose and fructose, are due to the different chemical bond of the monosaccharides. While the digestive enzymes cleave sucrose quite rapidly into glucose and fructose, this process takes longer with isomaltulose. Thus, a large part of the isomaltulose passes uncleaved through the upper portions of the small intestine where the GIP-producing K cells are found, which thus cannot substantially stimulate the GIP secretion. The GLP-1-producing L cells, by contrast, are found in the more distally located portions of the intestine and now due to the increased presence of glucose and fructose increasingly secrete the gut hormone. Furthermore, as previous studies of the scientists have shown, GIP may have an unfavorable effect on the metabolism and trigger fatty liver and inflammatory processes in adipose tissue. This suggests that the adverse effects of table sugar arise primarily from the hormone response, that is, they are induced by increased GIP secretion.

In summary, it can be said that isomaltulose in the intestine reduces GIP secretion, increases GLP-1 secretion, and at the same time preserves a certain measure of insulin secretion, thus preventing severe fluctuations in blood glucose levels. “This is particularly advantageous for people with type 2 diabetes since their blood glucose levels tend to get out of control. With regard to the regulation of the blood glucose metabolism, isomaltulose is therefore much better than common table sugar“, said the endocrinologist Pfeiffer, who heads the Department of Clinical Nutrition at DIfE. “However, it’s important to realize that it provides the same number of calories as other types of sugar. Moreover, it doesn’t taste as sweet, so you are tempted to eat more than you would with table sugar. If you don’t use the energy you consume, for example through sufficient physical activity, this will soon show up as weight gain,” Pfeiffer added. People who are overweight are more susceptible to cardiovascular disease and certain cancers and not least have a higher risk of type 2 diabetes. This has been confirmed in numerous studies, according to Pfeiffer. Therefore, the well-known adage also applies to isomaltulose: The dose makes the poison.

Background Information:

*GLP-1 and GIP:

Glucagon-like peptide-1 (GLP-1): In the intestine, L cells secrete GLP-1 after stimulation through carbohydrates (e.g. sugar), proteins or fats. The peptide hormone has a half-life of less than two minutes. It stimulates insulin secretion and at the same time inhibits the secretion of the hormone insulin antagonist glucagon. Both of these lead to a drop in blood glucose levels. Furthermore, studies indicate that it restores the insulin sensitivity of the beta cells in the pancreas and counteracts cell death. In addition, it delays the absorption of carbohydrates from the intestine and induces satiety (Source: Wikipedia).

Gastric inhibitory polypeptide (GIP): After food intake, the K cells in the small intestine secrete GIP. Evidence shows that the main function of GIP is to stimulate insulin secretion by the beta cells.
If the effect of GIP is inhibited through a high-fat diet, this counteracts the development of obesity and insulin resistance. In addition, scientists suspect that GIP plays a crucial role in the case of decreasing insulin action for the change of fat oxidation to fat storage. It could thus play an important role in the secondary prevention of insulin resistance. (Source: Wikipedia).

The German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE) is a member of the Leibniz Association. It investigates the causes of diet-related diseases in order to develop new strategies for prevention and therapy and to provide dietary recommendations. Its research focus includes the causes and consequences of the metabolic syndrome, which is a combination of obesity, high blood pressure, insulin resistance and lipid metabolism disorder, as well as the role of diet in healthy aging and the biological basis of food choices and eating habits. In addition, the DIfE is a partner of the German Center for Diabetes Research (DZD), which was founded in 2009 and has since been funded by the BMBF.

The Leibniz Association is the umbrella organization for 88 independent research institutions whose spectrum encompasses the natural, engineering and environmental sciences, economics, the spatial and social sciences as well as the humanities. Leibniz Institutes address issues of social, economic and ecological relevance. They conduct knowledge-driven and applied basic research, also in the overarching Leibniz research networks, as well as maintain scientific infrastructure and provide research-based services. The Leibniz Association sets priorities in knowledge transfer, in particular with the Leibniz research museums. It provides advice and information for policymakers, academia, business and industry and the general public. Leibniz Institutes collaborate intensively with universities – in the form of “Leibniz Science Campi” (thematic partnerships between university and non-university research institutes), for example – as well as with industry and other partners in Germany and abroad. They are subject to a standard-setting, transparent and independent evaluation procedure. Due to the importance of the Leibniz Institutes for Germany as a whole, they are funded jointly by the federal government and state governments, employing some 18,100 individuals, including 9,200 researchers. The overall budget of the institutes amounts to more than EUR 1.6 billion.

Contact:

Prof. Dr. Andreas F. H. Pfeiffer
Department of Clinical Nutrition
German Institute of Human Nutrition
Potsdam-Rehbruecke (DIfE)
Arthur-Scheunert-Allee 114-116
14558 Nuthetal/Germany
Phone: +49 (0)33200 88-2771
Phone: +49 (0)30 450514 422
email: afhp@dife.de
email: afhp@charite.de

Dr. Farnaz Keyhani-Nejad
Department of Clinical Nutrition
German Institute of Human Nutrition
Potsdam-Rehbruecke (DIfE)
Arthur-Scheunert-Allee 114-116
14558 Nuthetal/Germany
email: Keyhani-Nejad.Farnaz@dife.de

Media contact:

Dr. Gisela Olias
Head, Press and Public Relations
German Institute of Human Nutrition
Potsdam-Rehbruecke (DIfE)
Phone: +49 (0)33200 88-2278/-2335
email: olias@dife.de
or presse@dife.de
www.dife.de