PMID- 23952467
OWN - NLM
STAT- MEDLINE
DCOM- 20140121
LR  - 20181217
IS  - 1742-1241 (Electronic)
IS  - 1368-5031 (Linking)
VI  - 67
IP  - 9
DP  - 2013 Sep
TI  - Choice of early treatment regimen and impact on beta-cell preservation in type 2 
      diabetes.
PG  - 876-87
LID - 10.1111/ijcp.12154 [doi]
AB  - The progressive deterioration of glycaemic control in individuals with type 2 
      diabetes mellitus (T2DM) results from insulin resistance combined with the 
      ongoing loss of beta-cell function. Although it had been suggested that most beta-cell 
      dysfunction occurs after the development of T2DM, studies have documented a 
      substantial early loss of beta-cell function, particularly during the prediabetic 
      state. In patients diagnosed with T2DM, beta-cell function continues to decline 
      despite treatment with commonly prescribed antihyperglycaemic medications, and 
      ultimately exogenous insulin administration is required to maintain optimal 
      glycaemic control. Thus, interventions to address the early decline in beta-cell 
      function could potentially alter the course of T2DM, preventing or delaying its 
      onset and decreasing the incidence of complications. Original research and review 
      articles on this topic were identified in a PubMed search from January 2000 
      through August 2012. Data from prospective studies and clinical trials suggest 
      that lifestyle modifications and certain antihyperglycaemic medications, 
      including thiazolidinediones (TZDs), glucagon-like peptide-1 (GLP-1) agonists, 
      dipeptidyl peptidase-4 (DPP-4) inhibitors and insulin, may preserve or enhance 
      beta-cell function. The implication of current data is that early initiation of 
      lifestyle modifications and antihyperglycaemic agents that preserve beta-cell 
      function might reverse or delay progression to T2DM in those with prediabetes. 
      Moreover, improved beta-cell function may confer more durable glucose control and 
      perhaps reduce/delay the incidence of diabetic complications. Long-term studies 
      are needed to validate this hypothesis.
CI  - (c) Published 2013. This article is a U.S. Government work and is in the public 
      domain in the USA.
FAU - Mudaliar, S
AU  - Mudaliar S
AD  - Center for Metabolic Research, VA San Diego Healthcare System, San Diego, CA, 
      USA. smudaliar@vapop.ucsd.edu
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - India
TA  - Int J Clin Pract
JT  - International journal of clinical practice
JID - 9712381
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
SB  - IM
MH  - Decision Making
MH  - Diabetes Complications/complications/drug therapy
MH  - Diabetes Mellitus, Type 2/*drug therapy
MH  - Disease Progression
MH  - Early Diagnosis
MH  - Humans
MH  - Hypoglycemic Agents/*therapeutic use
MH  - Insulin/metabolism
MH  - Insulin Secretion
MH  - Insulin-Secreting Cells/*drug effects/physiology
MH  - Risk Reduction Behavior
EDAT- 2013/08/21 06:00
MHDA- 2014/01/22 06:00
CRDT- 2013/08/20 06:00
PHST- 2012/10/12 00:00 [received]
PHST- 2013/02/15 00:00 [accepted]
PHST- 2013/08/20 06:00 [entrez]
PHST- 2013/08/21 06:00 [pubmed]
PHST- 2014/01/22 06:00 [medline]
AID - 10.1111/ijcp.12154 [doi]
PST - ppublish
SO  - Int J Clin Pract. 2013 Sep;67(9):876-87. doi: 10.1111/ijcp.12154.