devazepide and Insulin-Resistance

devazepide has been researched along with Insulin-Resistance* in 1 studies

Other Studies

1 other study(ies) available for devazepide and Insulin-Resistance

Article	Year
Intestinal cholecystokinin controls glucose production through a neuronal network. Cell metabolism, 2009, Volume: 10, Issue:2 Cholecystokinin (CCK) is a peptide hormone that is released from the gut in response to nutrients such as lipids to lower food intake. Here we report that a primary increase of CCK-8, the biologically active form of CCK, in the duodenum lowers glucose production independent of changes in circulating insulin levels. Furthermore, we show that duodenal CCK-8 requires the activation of the gut CCK-A receptor and a gut-brain-liver neuronal axis to lower glucose production. Finally, duodenal CCK-8 fails to lower glucose production in the early onset of high-fat diet-induced insulin resistance. These findings reveal a role for gut CCK that lowers glucose production through a neuronal network and suggest that intestinal CCK resistance may contribute to hyperglycemia in response to high-fat feeding. Topics: Animals; Cholecystokinin; Devazepide; Dietary Fats; Duodenum; Glucose; Insulin; Insulin Resistance; Male; Nerve Net; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin A	2009

Article

Year

Intestinal cholecystokinin controls glucose production through a neuronal network.

Cell metabolism, 2009, Volume: 10, Issue:2

Cholecystokinin (CCK) is a peptide hormone that is released from the gut in response to nutrients such as lipids to lower food intake. Here we report that a primary increase of CCK-8, the biologically active form of CCK, in the duodenum lowers glucose production independent of changes in circulating insulin levels. Furthermore, we show that duodenal CCK-8 requires the activation of the gut CCK-A receptor and a gut-brain-liver neuronal axis to lower glucose production. Finally, duodenal CCK-8 fails to lower glucose production in the early onset of high-fat diet-induced insulin resistance. These findings reveal a role for gut CCK that lowers glucose production through a neuronal network and suggest that intestinal CCK resistance may contribute to hyperglycemia in response to high-fat feeding.

Topics: Animals; Cholecystokinin; Devazepide; Dietary Fats; Duodenum; Glucose; Insulin; Insulin Resistance; Male; Nerve Net; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin A

2009