PMID- 18200800
OWN - NLM
STAT- MEDLINE
DCOM- 20080225
LR  - 20211020
IS  - 1176-6344 (Print)
IS  - 1178-2048 (Electronic)
IS  - 1176-6344 (Linking)
VI  - 3
IP  - 6
DP  - 2007
TI  - A review of nateglinide in the management of patients with type 2 diabetes.
PG  - 797-807
AB  - Impaired insulin secretion occurs early in the pathogenesis of type 2 diabetes 
      mellitus (T2DM) and is chronic and progressive, resulting initially in impaired 
      glucose tolerance (IGT) and eventually in T2DM. As most patients with T2DM have 
      both insulin resistance and insulin deficiency, therapy for T2DM should aim to 
      control not only fasting, but also postprandial plasma glucose levels. While oral 
      glucose-lowering treatment with metformin and thiazolidinediones corrects fasting 
      plasma glucose, these agents do not address the problem of mealtime glucose 
      spikes that have been shown to trigger atherogenic processes. Nateglinide is a 
      derivative of the amino acid D-phenylalanine, which acts directly on the 
      pancreatic beta-cells to stimulate insulin secretion. Nateglinide monotherapy 
      controls significantly mealtime hyperglycemia and results in improved overall 
      glycemic control in patients with T2DM by reducing glycosylated hemoglobin 
      (HbA1c) levels. The combination of nateglinide with insulin-sensitising agents, 
      such as metformin and thiazolidinediones, targets both insulin deficiency and 
      insulin resistance and results in reductions in HbA1c that could not be achieved 
      by monotherapy with other antidiabetic agents. In prediabetic subjects with IGT, 
      nateglinide restores early insulin secretion and reduces postprandial 
      hyperglycemia. Nateglinide has an excellent safety and tolerability profile and 
      provides a lifetime flexibility that other antidiabetic agents could not 
      accomplish. The aim of this review is to identify nateglinide as an effective 
      "gate-keeper" in T2DM, since it restores early-phase insulin secretion and 
      prevents mealtime glucose spikes throughout the day and to evaluate the results 
      of ongoing research into its potential role in delaying the progression to overt 
      diabetes and reducing its complications and mortality.
FAU - Tentolouris, Nicholas
AU  - Tentolouris N
AD  - Ist Department of Propaedeutic Medicine,Athens University Medical School, Laiko 
      General Hospital, Athens, Greece. ntentol@med.uoa.gr
FAU - Voulgari, Christina
AU  - Voulgari C
FAU - Katsilambros, Nicholas
AU  - Katsilambros N
LA  - eng
PT  - Journal Article
PT  - Review
PL  - New Zealand
TA  - Vasc Health Risk Manag
JT  - Vascular health and risk management
JID - 101273479
RN  - 0 (Cyclohexanes)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (KATP Channels)
RN  - 41X3PWK4O2 (Nateglinide)
RN  - 47E5O17Y3R (Phenylalanine)
SB  - IM
MH  - Cyclohexanes/pharmacology/*therapeutic use
MH  - Diabetes Mellitus, Type 2/*drug therapy/prevention & control
MH  - Fasting
MH  - Humans
MH  - Hypoglycemic Agents/pharmacology/*therapeutic use
MH  - Insulin/metabolism
MH  - Insulin Secretion
MH  - KATP Channels/antagonists & inhibitors
MH  - Nateglinide
MH  - Phenotype
MH  - Phenylalanine/*analogs & derivatives/pharmacology/therapeutic use
MH  - Postprandial Period
PMC - PMC2350129
EDAT- 2008/01/19 09:00
MHDA- 2008/02/26 09:00
CRDT- 2008/01/19 09:00
PHST- 2008/01/19 09:00 [pubmed]
PHST- 2008/02/26 09:00 [medline]
PHST- 2008/01/19 09:00 [entrez]
PST - ppublish
SO  - Vasc Health Risk Manag. 2007;3(6):797-807.