
PMID- 26696678
OWN - NLM
STAT- PubMed-not-MEDLINE
DA  - 20151223
DCOM- 20160414
LR  - 20151223
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 39 Suppl 1
DP  - 2016 Jan
TI  - 4. Prevention or Delay of Type 2 Diabetes.
PG  - S36-8
LID - 10.2337/dc16-S007 [doi]
CN  - American Diabetes Association
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2015/12/24 06:00
MHDA- 2015/12/24 06:01
CRDT- 2015/12/24 06:00
AID - 39/Supplement_1/S36 [pii]
AID - 10.2337/dc16-S007 [doi]
PST - ppublish
SO  - Diabetes Care. 2016 Jan;39 Suppl 1:S36-8. doi: 10.2337/dc16-S007.

PMID- 19396026
OWN - NLM
STAT- MEDLINE
DA  - 20090427
DCOM- 20090521
LR  - 20090427
IS  - 1565-4753 (Print)
IS  - 1565-4753 (Linking)
VI  - 6
IP  - 3
DP  - 2009 Mar
TI  - Breakthroughs in monogenic diabetes genetics: from pediatric forms to young
      adulthood diabetes.
PG  - 405-17
AB  - Several monogenic forms of pancreatic beta-cell dysfunction leading to
      non-autoimmune diabetes have been diagnosed early in life, in neonates or during 
      infancy, in childhood or even in young adulthood, with genetically heterogeneous 
      aetiologies.They include neonatal diabetes mellitus, non auto-immune diabetes in 
      infancy and childhood, dominantly inherited young-onset diabetes and very rare
      diabetes-associated syndromes. More than ten genes that are highly expressed in
      the pancreatic beta-cell have been identified in these monogenic subtypes of
      diabetes, and several aetiological mechanisms of beta-cell dysfunction are
      involved including reduced beta-cell number, failure of glucose sensing and
      increased destruction of the beta-cell, which result in inadequate insulin
      secretion despite a chronic hyperglycemia. There is rising evidence that common
      polymorphisms in the genes implicated in monogenic diabetes may also be involved 
      in susceptibility to adulthood type 2 diabetes. This review describes the major
      advances arising from the identification of the genetic and molecular mechanisms 
      underlying the clinical features of various conditions of diabetes in the young, 
      and how these new genetic and biological insights led to novel pharmacogenomic
      approaches.
FAU - Vaxillaire, Martine
AU  - Vaxillaire M
AD  - CNRS UMR 8090, Institute of Biology & Pasteur Institute, Lille, France.
      martine.vaxillaire@good.ibl.fr
FAU - D, Pharm
AU  - D P
FAU - Bonnefond, Amelie
AU  - Bonnefond A
FAU - Froguel, Philippe
AU  - Froguel P
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Israel
TA  - Pediatr Endocrinol Rev
JT  - Pediatric endocrinology reviews : PER
JID - 101202124
SB  - IM
MH  - Adolescent
MH  - Child
MH  - Child, Preschool
MH  - Diabetes Mellitus/drug therapy/*genetics/metabolism
MH  - Diabetes Mellitus, Type 1/drug therapy/genetics
MH  - Diabetes Mellitus, Type 2/drug therapy/genetics
MH  - Genetic Predisposition to Disease
MH  - Genetic Variation
MH  - Humans
MH  - Hyperglycemia/drug therapy/genetics/metabolism
MH  - Infant
MH  - Infant, Newborn
MH  - Young Adult
RF  - 98
EDAT- 2009/04/28 09:00
MHDA- 2009/05/22 09:00
CRDT- 2009/04/28 09:00
PST - ppublish
SO  - Pediatr Endocrinol Rev. 2009 Mar;6(3):405-17.

PMID- 18028440
OWN - NLM
STAT- MEDLINE
DA  - 20080222
DCOM- 20080411
LR  - 20080222
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 25
IP  - 2
DP  - 2008 Feb
TI  - The islet autoantibody titres: their clinical relevance in latent autoimmune
      diabetes in adults (LADA) and the classification of diabetes mellitus.
PG  - 117-25
AB  - Latent autoimmune diabetes in the adult (LADA) is a slowly progressive form of
      autoimmune diabetes, characterized by diabetes-associated autoantibody
      positivity. A recent hypothesis proposes that LADA consists of a heterogeneous
      population, wherein several subgroups can be identified based on their autoimmune
      status. A systematic review of the literature was carried out to appraise whether
      the clinical characteristics of LADA patients correlate with the titre and
      numbers of diabetes-associated autoantibodies. We found that the simultaneous
      presence of multiple autoantibodies and/or a high-titre anti-glutamic acid
      decarboxylase (GAD)--compared with single and low-titre autoantibody--is
      associated with an early age of onset, low fasting C-peptide values as a marker
      of reduced pancreatic B-cell function, a high predictive value for future insulin
      requirement, the presence of other autoimmune disorders, a low prevalence of
      markers of the metabolic syndrome including high body mass index, hypertension
      and dyslipidaemia, and a high prevalence of the genotype known to increase the
      risk of Type 1 diabetes. We propose a more continuous classification of diabetes 
      mellitus, based on the finding that the clinical characteristics gradually change
      from classic Type 1 diabetes to LADA and finally to Type 2 diabetes. Future
      studies should focus on determining optimal cut-off points of anti-GAD for
      differentiating clinically relevant diabetes mellitus subgroups.
FAU - van Deutekom, A W
AU  - van Deutekom AW
AD  - Department of Endocrinology/Diabetes Center, VU University Medical Center,
      Amsterdam, The Netherlands.
FAU - Heine, R J
AU  - Heine RJ
FAU - Simsek, S
AU  - Simsek S
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20071119
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
RN  - 0 (Autoantibodies)
RN  - 0 (C-Peptide)
RN  - EC 4.1.1.15 (Glutamate Decarboxylase)
SB  - IM
MH  - Adult
MH  - Autoantibodies/*blood
MH  - Body Mass Index
MH  - C-Peptide/blood
MH  - Diabetes Mellitus, Type 1/*immunology/metabolism
MH  - Female
MH  - Glutamate Decarboxylase/*immunology
MH  - Humans
MH  - Islets of Langerhans/*immunology/physiopathology
MH  - Male
MH  - Middle Aged
RF  - 95
EDAT- 2007/11/22 09:00
MHDA- 2008/04/12 09:00
CRDT- 2007/11/22 09:00
AID - DME2316 [pii]
AID - 10.1111/j.1464-5491.2007.02316.x [doi]
PST - ppublish
SO  - Diabet Med. 2008 Feb;25(2):117-25. Epub 2007 Nov 19.
