*Mitigating Diabetic Foot Ulcers: The Effect of Diet and Microbiome DOI: http://dx.doi.org/10.5772/intechopen.106629*

glycogen, or stimulated by incretins to be digested and absorbed into adipocytes and stored as fat (see **Figure 1**).

Incretins also stimulate the release of insulin as well and as incretin levels rise because of overeating, insulin levels rise as well. GLP-1 is released from L-cells of the small intestine [16]. One of the effects of increased secretion of insulin however can cause insulin receptors to desensitize and become nonresponsive and promoting insulin resistance. This leads to high blood glucose levels leading to diabetes. Increased amounts of insulin, incretin agonists, DTT inhibitors, and other drugs are

#### **Figure 1.**

*Represented above is a simplified diagram of blood glycemic control and fat deposition. Incretins are at the heart of control and not just involved in stimulating insulin release. Incretins can have direct effects on fat deposition. In the energy balance mode and carbohydrate – insulin model of obesity it appears the influence of diet and SCFAs are not emphasized enough on the impact of glycemic control and fat deposition. Microbiota and the production of SCFAs have a profound effect on insulin release. Although carbohydrates have a large effect on secretion of insulin, other nutrients also have an effect. Although insulin can stimulate the production fat in adipocytes, incretins and SCFAs can have a direct effect as well.*

designed to increase the amounts of insulin without fixing the underlying physiological causes. For TTDM and similar forms of diabetes, this is possible but for TT1 this is more difficult and in most cases impossible. So, depending on the cause, the diets and effects of microbiota are quite different.

GLP-1 and GIP both stimulate the secretion of insulin from the Beta cells of the Pancreas, yet they have different effects on obesity and fat deposition and different studies are making the functions unclear [17]. GLP-1 directly inhibits appetite and food intake and GLP-1 antagonists have been developed into drugs that can help glycemic control. GIP however lacks these functions and although some studies have used agonists to reduce weight gain, also antagonists have shown the same effect [17–20]. In addition, GIP receptor knockout mice fail to gain weight even when fed a high-fat diet [21]. GIP is released when glucose and proteins are absorbed which then promote additional absorption [22, 23].

Incretin control is what causes insulin release and increased amounts can lead to diabetes and eventually the complications that eventually lead to foot ulcers. Rises in incretins particularly GIP can contribute to weight gain by increasing absorption of nutrients and fat deposition (**Figure 1**). Control of incretin release could modulate and maintain controlled diabetes and less of a risk of ulcers. Even before one eats a meal, incretins such as GLP-1 and GIP are released in anticipation of glucose absorption. But the evidence is rather ambiguous [24]. Some studies show that even the sweet taste of food (even if it's an artificial sweetener) can trigger incretin release during the cephalic phase of digestion [1, 25]. Others have shown no release of insulin during the cephalic phase [26, 27].
