Dietary starch is usually associated with elevated postprandial glycemic response. This is a potential risk factor of type 2 diabetes. Here, a 1,4-α-glucan branching enzyme (GBE) was employed to reassemble α-1,4 and α-1,6 glycosidic bonds in starch molecules. Structural characterization showed that GBE-catalyzed molecular reassembly created an innovative short-clustered maltodextrin (SCMD), which showed a dense internal framework along with shortened external chains. Such short-clustered molecules obstructed digestive enzymes attack and displayed dramatically reduced digestibility. Therefore, SCMD was served as a dietary starch substitute to improve postprandial glucose homeostasis. A 22.3% decrease in glycemic peak was therefore detected in ICR mice following SCMD intake (10.7 mmol/L), compared with that in the control (13.8 mmol/L). Moreover, an attenuated insulin response (40.5% lower than that in control) to SCMD intake was regarded suitable for diabetes management. These novel discoveries demonstrate that enzymatically rebuilding starch molecules may be a meaningful strategy for diabetes management.

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Molecular structure of starch in daily diet is closely associated with diabetes management. By enzymatically reassembling α-1,4 and α-1,6 glycosidic bonds in starch molecules, we have synthesized an innovative short-clustered maltodextrin (SCMD) which slowly releases glucose during digestion. Here, we investigated the potential benefits of the SCMD-containing diet using diabetic db/db mice. As compared to a diet with normal starch, this dietary style greatly attenuated hyperglycemia and repaired symptoms associated with diabetes. Additionally, in comparison with acarbose (an α-glucosidase inhibitor) administration, the SCMD-containing diet more effectively accelerated brown adipose activation and improved energy metabolism of db/db mice. Furthermore, the SCMD-containing diet was a more suitable approach to improving the intestinal microflora than acarbose administration, especially the proliferation of Mucispirillum, Akkermansia, and Bifidobacterium. These results reveal a novel strategy for diabetes management based on enzymatically rebuilding starch molecules in the daily diet.

Reconstructing molecular structure is an effective approach to attenuating glycemic response to starch. Previously, we rearranged α-1,4 and α-1,6-glycosidic bonds in starch molecules to produce short-clustered maltodextrin (SCMD). The present study revealed that SCMD slowly released glucose until the distal ileum. The activated ileal glucose-sensing enabled SCMD to be a potent inducer for glucagon-like peptide-1 (GLP-1). Furthermore, SCMD was found feasible to serve as the dominant dietary carbohydrate to rescue mice from diabetes. Interestingly, a mixture of normal maltodextrin and resistant dextrin (MD+RD), although it caused an attenuated glycemic response similar to that of SCMD, failed to ameliorate glucose homeostasis because it hardly induced GLP-1 secretion. The serum GLP-1 levels seen in MD+RD-fed mice (5.25 ± 1.51 pmol/L) were significantly lower than those seen in SCMD-fed mice (8.25 ± 2.01 pmol/L, p < 0.05). Further investigation revealed that the beneficial effects of SCMD could be abolished by a GLP-1 receptor (GLP-1R) antagonist. These results identify GLP-1R signaling as a critical contributor to SCMD-exerted health benefits and highlight the role of ileal glucose-sensing in designing dietary carbohydrates.