Ablation of Ghrelin O-Acyltransferase Does Not Improve Glucose Intolerance or Body Adiposity in Mice on a Leptin-Deficient ob/ob Background

Autor: Henriette Kirchner, Matthias H. Tschöp, Jenna Holland, Dhiraj G. Kabra, Paul T. Pfluger, Kristy M. Heppner
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Leptin
Male
Anatomy and Physiology
Mouse
Acylation
medicine.medical_treatment
Mice
Obese

lcsh:Medicine
Gene Knockout Techniques
Mice
Endocrinology
0302 clinical medicine
Homeostasis
Glucose homeostasis
lcsh:Science
Adiposity
Mice
Knockout

0303 health sciences
Multidisciplinary
Leptin Deficiency
digestive
oral
and skin physiology

Animal Models
Ghrelin
Ghrelin O-acyltransferase
3. Good health
Phenotype
Medicine
Female
hormones
hormone substitutes
and hormone antagonists

Research Article
medicine.medical_specialty
Endocrine System
030209 endocrinology & metabolism
Carbohydrate metabolism
Biology
03 medical and health sciences
Model Organisms
Internal medicine
Glucose Intolerance
medicine
Animals
Obesity
030304 developmental biology
Diabetic Endocrinology
Endocrine Physiology
Insulin
Body Weight
lcsh:R
Membrane Proteins
Diabetes Mellitus Type 2
Hormones
Glucose
lcsh:Q
Physiological Processes
Protein Processing
Post-Translational

Acyltransferases
Zdroj: PLoS ONE; Vol 8
PLoS ONE 8:e61822 (2013)
PLoS ONE
PLoS ONE, Vol 8, Iss 4, p e61822 (2013)
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0061822
Popis: Type 2 Diabetes is a global health burden and based on current estimates will become an even larger problem in the future. Developing new strategies to prevent and treat diabetes is a scientific challenge of high priority. The stomach hormone ghrelin has been associated with playing a role in the regulation of glucose homeostasis. However, its precise mechanism and impact on whole glucose metabolism remains to be elucidated. This study aims to clarify the role of the two ghrelin isoforms acyl- and desacyl ghrelin in regulating glucose homeostasis. Therefore ghrelin activating enzyme Ghrelin-O-acyltransferase (GOAT) was ablated in leptin-deficient ob/ob mice to study whether specific acyl ghrelin deficiency or desacyl ghrelin abundance modifies glucose tolerance on a massively obese background. As targeted deletion of acyl ghrelin does not improve glucose homeostasis in our GOAT-ob/ob mouse model we conclude that neither acyl ghrelin nor the increased ratio of desacyl/acyl ghrelin is crucial for controlling glucose homeostasis in the here presented model of massive obesity induced by leptin deficiency.
Databáze: OpenAIRE