PMID- 15925013
OWN - NLM
STAT- MEDLINE
DCOM- 20050916
LR  - 20220331
IS  - 0188-4409 (Print)
IS  - 0188-4409 (Linking)
VI  - 36
IP  - 3
DP  - 2005 May-Jun
TI  - Regulation of plasma triglycerides in insulin resistance and diabetes.
PG  - 232-40
AB  - Increased plasma levels of triglycerides (TG) in very low density lipoproteins 
      (VLDL) are not only common characteristics of the dyslipidemia associated with 
      insulin resistance and type 2 diabetes mellitus (T2DM) but are the central 
      pathophysiologic feature of the abnormal lipid profile. Overproduction of VLDL 
      leads to increased plasma levels of TG which, via an exchange process mediated by 
      cholesterol ester transfer protein (CETP), results in low levels of high density 
      lipoprotein (HDL) cholesterol and apolipoprotein A-I, and the generation of 
      small, dense, cholesterol ester depleted low density lipoproteins (LDL). 
      Increased assembly and secretion of VLDL by the liver results from the complex, 
      post-transcriptional regulation of apolipoprotein B (apoB) metabolism in the 
      liver. In the presence of low levels of hepatic TG and cholesterol, much of the 
      constitutively synthesized apoB is degraded by both proteasomal and 
      non-proteasomal pathways. When excess TG, and to a lesser extent, cholesterol, 
      are present, and in the presence of active microsomal triglycerides transfer 
      protein, apoB is targeted for secretion. The major sources of TG in the liver: 
      uptake of fatty acids (FA) released by lipolysis of adipose tissue TG, uptake of 
      TGFA in VLDL and chylomicrons remnants, and hepatic de novo lipogenesis (the 
      synthesis of FA from glucose) are all abnormally increased in insulin resistance. 
      Treatment of the dyslipidemia in insulin resistant individuals and patients with 
      T2DM has been successful in reducing cardiovascular disease; LDL cholesterol, TG, 
      and HDL cholesterol are all appropriate targets for therapy when diet, exercise, 
      and weight loss do not achieve goals.
FAU - Ginsberg, Henry N
AU  - Ginsberg HN
AD  - College of Physicians and Surgeons of Columbia University, New York, NY 10032, 
      USA. hng1@columbia.edu
FAU - Zhang, Yuan-Li
AU  - Zhang YL
FAU - Hernandez-Ono, Antonio
AU  - Hernandez-Ono A
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Arch Med Res
JT  - Archives of medical research
JID - 9312706
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Apolipoproteins B)
RN  - 0 (Chylomicrons)
RN  - 0 (Fatty Acids)
RN  - 0 (Lipoproteins)
RN  - 0 (Lipoproteins, HDL)
RN  - 0 (Lipoproteins, VLDL)
RN  - 0 (Triglycerides)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Apolipoprotein A-I/metabolism
MH  - Apolipoproteins B/metabolism
MH  - Cholesterol/metabolism
MH  - Chylomicrons/metabolism
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Fatty Acids/metabolism
MH  - Humans
MH  - *Insulin Resistance
MH  - Lipid Metabolism
MH  - Lipoproteins/metabolism
MH  - Lipoproteins, HDL/metabolism
MH  - Lipoproteins, VLDL/chemistry
MH  - Liver/metabolism
MH  - Models, Biological
MH  - Triglycerides/*blood
RF  - 53
EDAT- 2005/06/01 09:00
MHDA- 2005/09/17 09:00
CRDT- 2005/06/01 09:00
PHST- 2004/11/27 00:00 [received]
PHST- 2004/11/27 00:00 [accepted]
PHST- 2005/06/01 09:00 [pubmed]
PHST- 2005/09/17 09:00 [medline]
PHST- 2005/06/01 09:00 [entrez]
AID - S0188-4409(05)00006-8 [pii]
AID - 10.1016/j.arcmed.2005.01.005 [doi]
PST - ppublish
SO  - Arch Med Res. 2005 May-Jun;36(3):232-40. doi: 10.1016/j.arcmed.2005.01.005.