ArticleDiabetologia2012
Ectopic expression of glucagon receptor in skeletal muscles improves glucose homeostasis in a mouse model of diabetes.
Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Integration of metabolic flux with hepatic glucagon signaling and gene expression profiles in the conscious dog.American journal of physiology. Endocrinology and metabolism · 2024Article
- Antagonistic interaction between Nodal and insulin modulates pancreatic β-cell proliferation and survival.Cell communication and signaling : CCS · 2018Article
- HDAC5 integrates ER stress and fasting signals to regulate hepatic fatty acid oxidation.Journal of lipid research · 2018Article
- Current insights and new perspectives on the roles of hyperglucagonemia in non-insulin-dependent type 2 diabetes.Current hypertension reports · 2013Review
- Intra-islet glucagon secretion and action in the regulation of glucose homeostasis.Frontiers in physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
aims/hypothesisExcessive secretion of glucagon partially contributes to the development of diabetic hyperglycaemia. However, complete blocking of glucagon action will lead to adverse effects, since glucagon exerts certain beneficial effects via its receptor in many organs. We aimed to study the effects of a 'decoy receptor' for circulating glucagon on modulating beta cell function and glucose homeostasis in mice by over-producing the glucagon receptor (GCGR) in skeletal muscles.
methodsWe generated transgenic mice in which the expression of Gcgr is driven by the muscle specific creatine kinase (Mck) promoter, and assessed the effects of glucagon on the modulation of glucose homeostasis under conditions of extremes of glucose influx or efflux.
resultsMck/Gcgr mice showed increased circulating levels of glucagon and insulin, resulting in an unchanged ratio of glucagon-to-insulin. The levels of hepatic glucose-6-phosphatase (G6PC) and fructose-1,6-bisphosphatase (F1,6P2ase) were significantly decreased, whereas the phosphorylation level of pancreatic cAMP-response-element-binding-protein (CREB) was significantly increased in these transgenic mice. Under basal conditions, the mice displayed normal blood glucose levels and unchanged glucose tolerance and insulin sensitivity when compared with their age-matched wild-type (WT) littermates. However, following multiple low-dose streptozotocin injections, Mck/Gcgr mice exhibited a delay in the onset of hyperglycaemia compared with the WT controls. This was associated with preserved beta cell mass and beta cell secretory capacity in response to glucose challenge. CONCLUSIONS/
interpretationWe suggest that mild and chronic hyperglucagonaemia, through a strategy involving neutralising peripheral glucagon action, provides beneficial effects on beta cell function and glucose homeostasis. Mck/Gcgr mice thus represent a novel mouse model for studying the physiological effects of glucagon.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.