PMID- 28982341
OWN - NLM
STAT- MEDLINE
DCOM- 20180718
LR  - 20180718
IS  - 2212-3873 (Electronic)
IS  - 1871-5303 (Linking)
VI  - 17
IP  - 4
DP  - 2017 Nov 16
TI  - Gastrin - A Potential Predictor of Response to Incretin Therapy in Diabetes Type 
      2 Patients.
PG  - 297-302
LID - 10.2174/1871530317666171003162104 [doi]
AB  - BACKGROUND AND OBJECTIVES: Personalized management of diabetes has become an 
      imperative since majority of monotherapy fails within 3 years of its use. 
      Identifying responders from nonresponders for a certain type of therapy would 
      reduce a period of unsuccessful treatment and minimize health care costs. 
      Incretin therapies, mainly glucagon-like peptide (GLP)-1 receptor agonists (GLP- 
      1RA) are relatively new glucose-lowering agents which increase insulin and lower 
      glucagon response as well as slow down glucose absorption by acting on gastric 
      emptying. However, problem with incretin- based therapy is distinguishing 
      responders from non-responders and currently lack of specific predictors of 
      treatment response. DISCUSSION: Experimental data demonstrated that activation of 
      GLP-1 and gastrin signaling induces beta cell neogenesis, leading to 
      glucose-dependent insulin secretion. Several studies demonstrated better glycemic 
      control in patients with type 2 diabetes (DMT2) co-treated with proton pump 
      inhibitors (PPI) and incretin based therapy agents. CONCLUSION: Higher gastrin 
      levels in patients with diabetes prior to initiation of treatment with incretin 
      mimetics could suggest a better potential for reversible human beta-cell 
      reprogramming with concomitant incretin therapy. Therefore, baseline levels of 
      endogenous gastrin could be used as a predictor of response to GLP-1 therapy. In 
      addition, treatment with PPI could also raise gastrin levels and in patients 
      treated with GLP-1RA, lead to better glycemic control by initiating beta-cell 
      neogenesis and proliferation of pancreatic beta-cells.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.org.
FAU - Bilic-Curcic, Ines
AU  - Bilic-Curcic I
AD  - Department of Pharmacology, Faculty of Medicine, J.J.Strossmayer University 
      Osijek, Clinical Hospital Center Osijek, Osijek, Croatia.
FAU - Berkovic, Maja C
AU  - Berkovic MC
AD  - Department of Endocrinology, Diabetes and Metabolism, University Hospital Centre 
      Sestre milosrdnice, Zagreb, Croatia.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Endocr Metab Immune Disord Drug Targets
JT  - Endocrine, metabolic & immune disorders drug targets
JID - 101269157
RN  - 0 (Biomarkers)
RN  - 0 (Gastrins)
RN  - 0 (Incretins)
SB  - IM
MH  - B-Lymphocytes/drug effects/metabolism
MH  - Biomarkers/blood
MH  - Diabetes Mellitus, Type 2/*blood/diagnosis/*drug therapy
MH  - Gastrins/*blood
MH  - Humans
MH  - Incretins/pharmacology/*therapeutic use
MH  - Predictive Value of Tests
MH  - Treatment Outcome
OTO - NOTNLM
OT  - Diabetes mellitus
OT  - GLP-1RA
OT  - gastrin
OT  - incretin therapy
OT  - personalized treatment
OT  - beta-cell preservation
EDAT- 2017/10/07 06:00
MHDA- 2018/07/19 06:00
CRDT- 2017/10/07 06:00
PHST- 2017/07/19 00:00 [received]
PHST- 2017/09/20 00:00 [revised]
PHST- 2017/09/27 00:00 [accepted]
PHST- 2017/10/07 06:00 [pubmed]
PHST- 2018/07/19 06:00 [medline]
PHST- 2017/10/07 06:00 [entrez]
AID - EMIDDT-EPUB-86168 [pii]
AID - 10.2174/1871530317666171003162104 [doi]
PST - ppublish
SO  - Endocr Metab Immune Disord Drug Targets. 2017 Nov 16;17(4):297-302. doi: 
      10.2174/1871530317666171003162104.