2016
DOI: 10.1016/j.bbrc.2016.01.115
|View full text |Cite
|
Sign up to set email alerts
|

d-chiro-inositol glycan reduces food intake by regulating hypothalamic neuropeptide expression via AKT-FoxO1 pathway

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
10
0

Year Published

2017
2017
2023
2023

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 12 publications
(10 citation statements)
references
References 30 publications
0
10
0
Order By: Relevance
“…However, data supporting the beneficial influence of DCI in the regulation of body mass, through the central regulation of food intake can be found. Jeon et al [63] demonstrated the effect of DCI on hypothalamic insulin signaling, by increasing the expression of anorexigenic neuropeptides (proopiomelanocortin) and orexigenic reduction (neuropeptide Y). After injection of DCI derivative, the intake of food and body weight in mice decreased [63].…”
Section: Cyclitols Insulin Resistance and Diabetesmentioning
confidence: 99%
“…However, data supporting the beneficial influence of DCI in the regulation of body mass, through the central regulation of food intake can be found. Jeon et al [63] demonstrated the effect of DCI on hypothalamic insulin signaling, by increasing the expression of anorexigenic neuropeptides (proopiomelanocortin) and orexigenic reduction (neuropeptide Y). After injection of DCI derivative, the intake of food and body weight in mice decreased [63].…”
Section: Cyclitols Insulin Resistance and Diabetesmentioning
confidence: 99%
“…injection of insulin can inhibit food intake through the regulation of PI3K signaling in the hypothalamus [14]. Moreover, in the hypothalamus, the forehead box-containing protein of the O subfamily (FoxO)1—a downstream transcription factor of the insulin-signaling pathway—has a dual function: inhibiting the expression of POMC and stimulating the expression of NPY leading to an increased food intake [15, 16]. On the other hand, FoxO1 activities are also regulated by the InsR/PI3K/Akt signaling pathway, in which insulin induces Akt phosphorylation, followed by inactivation of FoxO1 due to its phosphorylation by p-Akt [17].…”
Section: Introductionmentioning
confidence: 99%
“…GLK in hypothalamic neurons participates in glucose-sensing mechanisms and in triggering counter-regulatory responses in hypoglycemia, 49 while hypothalamic INSRA may have a satiety effect, 50 possibly modulating the AKT-(FOXO1) signaling pathway. 51 FOXO1, also participates in leptin signaling in the brain. 52 Gene expression in response to high continuous levels of prolactin was time-and region-dependent.…”
Section: Discussionmentioning
confidence: 99%