PMID- 20382838
OWN - NLM
STAT- MEDLINE
DCOM- 20100824
LR  - 20181217
IS  - 1945-1997 (Electronic)
IS  - 0098-6151 (Linking)
VI  - 110
IP  - 3 Suppl 2
DP  - 2010 Mar
TI  - Pathophysiology of type 2 diabetes: targeting islet cell dysfunction.
PG  - S2-7
AB  - Type 2 diabetes mellitus (T2DM) continues to be a major health problem worldwide. 
      It is well known that T2DM is a metabolic disorder characterized by 
      hyperglycemia, which arises from insufficient pancreatic insulin secretion, 
      insulin resistance in peripheral tissues, and inadequate suppression of glucagon 
      production. This suppression results in inadequate uptake, storage, and disposal 
      of ingested glucose accompanied by elevated hepatic production of glucose and 
      profound hyperglycemia. Notably, these pathophysiologic processes can progress to 
      a clinically significant degree even in patients with impaired glucose tolerance. 
      As researchers begin to unravel the genetic basis of T2DM, the gradual 
      accumulation of genetic polymorphisms in multiple genes-rather than the mutation 
      of a single "diabetes gene"-appears to be the driving force behind the increase 
      in T2DM risk. Emergent therapies for the management of T2DM include 
      incretin-based agents, which can effectively target two key processes in T2DM by 
      augmenting insulin secretion and inhibiting glucagon production.
FAU - Spellman, Craig W
AU  - Spellman CW
AD  - Department of Internal Medicine, Texas Tech University Health Sciences Center, 
      Odessa, TX 79763-4206, USA. craig.spellman@ttuhsc.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Am Osteopath Assoc
JT  - The Journal of the American Osteopathic Association
JID - 7503065
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Insulin)
RN  - 9007-92-5 (Glucagon)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Blood Glucose/metabolism
MH  - Diabetes Mellitus, Type 2/epidemiology/genetics/*physiopathology
MH  - Dietary Carbohydrates/administration & dosage/metabolism
MH  - Disease Progression
MH  - Endocrine Cells
MH  - Genetic Predisposition to Disease
MH  - Global Health
MH  - Glucagon/antagonists & inhibitors/biosynthesis/blood
MH  - Glucose/administration & dosage/metabolism
MH  - Humans
MH  - Incidence
MH  - Insulin/blood/metabolism
MH  - Insulin Resistance
MH  - Insulin Secretion
MH  - Insulin-Secreting Cells/*metabolism/pathology
MH  - Risk Assessment
RF  - 23
EDAT- 2010/04/23 06:00
MHDA- 2010/08/25 06:00
CRDT- 2010/04/13 06:00
PHST- 2010/04/13 06:00 [entrez]
PHST- 2010/04/23 06:00 [pubmed]
PHST- 2010/08/25 06:00 [medline]
AID - 110/3_suppl_2/S2 [pii]
PST - ppublish
SO  - J Am Osteopath Assoc. 2010 Mar;110(3 Suppl 2):S2-7.