Screening for Food Insecurity in a Pediatric Diabetes Program: Provider and Parent/Guardian Perspectives.

Food insecurity (FI) is associated with poor health outcomes in children, and studies have shown higher FI among children with diabetes mellitus. This study assessed provider (N = 22, 35.5% response rate) and parent/guardian (N = 207, 14.6% response rate) perspectives toward FI screening in a pediatric diabetes program. Among 22 providers, most "rarely" (54.5%) or "never" (27.3%) screened for FI although all felt that screening was at least "slightly important." Barriers included lack of time (63.6%), not remembering to screen (59.1%), lack of knowledge about how to address positive screens (45.5%), and being unsure how to screen (40.9%). Among 186 parent/guardians, only 24.1% had been asked about FI at a pediatric medical appointment, but only 8.6% disliked the idea of being asked by a medical provider at endocrinology visits. To be effective and sustainable, FI screening must fit within the visit flow, and providers need education on how to address positive screens.

Glucose elicits cephalic-phase insulin release in mice by activating KATP channels in taste cells.

The taste of sugar elicits cephalic-phase insulin release (CPIR), which limits the rise in blood glucose associated with meals. Little is known, however, about the gustatory mechanisms that trigger CPIR. We asked whether oral stimulation with any of the following taste stimuli elicited CPIR in mice: glucose, sucrose, maltose, fructose, Polycose, saccharin, sucralose, AceK, SC45647, or a nonmetabolizable sugar analog. The only taste stimuli that elicited CPIR were glucose and the glucose-containing saccharides (sucrose, maltose, Polycose). When we mixed an α-glucosidase inhibitor (acarbose) with the latter three saccharides, the mice no longer exhibited CPIR. This revealed that the carbohydrates were hydrolyzed in the mouth, and that the liberated glucose triggered CPIR. We also found that increasing the intensity or duration of oral glucose stimulation caused a corresponding increase in CPIR magnitude. To identify the components of the glucose-specific taste-signaling pathway, we examined the necessity of Calhm1, P2X2+P2X3, SGLT1, and Sur1. Among these proteins, only Sur1 was necessary for CPIR. Sur1 was not necessary, however, for taste-mediated attraction to sugars. Given that Sur1 is a subunit of the ATP-sensitive K+ channel (KATP) channel and that this channel functions as a part of a glucose-sensing pathway in pancreatic ß-cells, we asked whether the KATP channel serves an analogous role in taste cells. We discovered that oral stimulation with drugs known to increase (glyburide) or decrease (diazoxide) KATP signaling produced corresponding changes in glucose-stimulated CPIR. We propose that the KATP channel is part of a novel signaling pathway in taste cells that mediates glucose-induced CPIR.