ArticleJournal of molecular neuroscience : MN2012
Compensatory recovery of blood glucose levels in KKA(y) mice fed a high-fat diet: insulin-sparing effects of PACAP overexpression in β cells.
Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Protective Effects of PACAP in Diabetic Complications: Retinopathy, Nephropathy and Neuropathy.International journal of molecular sciences · 2025Review
- Hypoglycemia, Vascular Disease and Cognitive Dysfunction in Diabetes: Insights from Text Mining-Based Reconstruction and Bioinformatics Analysis of the Gene Networks.International journal of molecular sciences · 2021Article
- PACAP: A regulator of mammalian reproductive function.Molecular and cellular endocrinology · 2020Review
- Selenoprotein F knockout leads to glucose and lipid metabolism disorders in mice.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
- Comparative gene expression profiles in pancreatic islets associated with agouti yellow mutation and PACAP overexpression in mice.Biochemistry and biophysics reports · 2015Article
- The two faces of miR-29.Journal of cardiovascular medicine (Hagerstown, Md.) · 2015Review
- Chronic glucokinase activator treatment at clinically translatable exposures gives durable glucose lowering in two animal models of type 2 diabetes.British journal of pharmacology · 2014Article
- PACAP Inhibits β-cell Mass Expansion in a Mouse Model of Type II Diabetes: Persistent Suppressive Effects on Islet Density.Frontiers in endocrinology · 2013Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inadequate compensatory insulin secretion is observed during the development of type 2 diabetes and deteriorates over time in a manner that is difficult to reverse. Here, we found that plasma glucose levels in genetically diabetic KKA(y) mice fed a high-fat diet were markedly increased in young mice. However, the levels started to decrease at 22 weeks of age and returned to normal levels at around 40 weeks of age. These changes were accompanied by a marked increase in insulin levels from week 25 onwards. Decreased energy intake and suppressed fat pad accumulation were observed at 44-45 weeks of age compared with those at 19-22 weeks of age. β cell-specific overexpression of pituitary adenylate cyclase-activating polypeptide (PACAP), an insulinotropic neuropeptide, decreased the insulin levels required to compensate for hyperglycemia. Glucose disposal was significantly enhanced despite impaired insulin sensitivity in 41-44-week-old A(y) mice without or with PACAP overexpression. In conclusion, the present results provide further evidence that PACAP is involved in the regulation of hyperinsulinemia and islet hyperplasia in type 2 diabetes. Our results also indicate that A(y) mice fed a high-fat diet constitute an animal model suitable to study compensatory islet hyperplasia.
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