PMID- 19588729
OWN - NLM
STAT- MEDLINE
DCOM- 20090729
LR  - 20211020
IS  - 1138-7548 (Print)
IS  - 1138-7548 (Linking)
VI  - 65
IP  - 1
DP  - 2009 Mar
TI  - High lipolytic activity and dyslipidemia in a spontaneous hypertensive/NIH 
      corpulent (SHR/N-cp) rat: a genetic model of obesity and type 2 diabetes 
      mellitus.
PG  - 33-41
AB  - In order to better understand the link between obesity and type 2 diabetes, 
      lipolysis and its adrenergic regulation was investigated in various adipose 
      depots of obese adult females SHR/N-cp rats. Serum insulin, glucose, free fatty 
      acids (FFA), triglycerides (TG) and glycerol were measured. Adipocytes were 
      isolated from subcutaneous (SC), parametrial (PM) and retroperitoneal (RP) fat 
      pads. Total cell number and size, basal lipolysis or stimulated by norepinephrine 
      (NE) and BRL 37344 were measured in each depot. Obese rats were hyperinsulinemic 
      and hyperglycemic, suggesting high insulin resistance. They presented a marked 
      dyslipidemia, attested by increased serum FFA and TG levels. High serum glycerol 
      levels also suggest a strong lipolytic rate. Obese rats showed an excessive 
      development of all fat pads although a more pronounced effect was observed in the 
      SC one. The cellularity of this depot was increased 8 fold when compared to lean 
      rats, but these fat cells were only 1.5 to 2-fold larger. SC adipocytes showed a 
      marked increase in their basal lipolytic activity but a lack of change in 
      responsiveness to NE or BRL 37344. The association between high basal lipolysis 
      and increased cellularity yields to a marked adipose cell lipolytic rate, 
      especially from the SC region. SHR/N-cp rats were characterized by a hyperplasic 
      type of obesity with an excessive development of the SC depot. The dyslipidemia, 
      attested by an altered serum lipid profile could be attributed to excessive 
      lipolysis that contributes to increased FFA levels, and to early development of 
      insulin resistance through a lipotoxicity effect.
FAU - Atgie, C
AU  - Atgie C
AD  - Department of University Sciences (DUSA), Bordeaux 1 University, Bordeaux, 
      France. claude.atgie@u-bordeaux1.fr
FAU - Hadj-Sassi, A
AU  - Hadj-Sassi A
FAU - Bukowiecki, L
AU  - Bukowiecki L
FAU - Mauriege, P
AU  - Mauriege P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Spain
TA  - J Physiol Biochem
JT  - Journal of physiology and biochemistry
JID - 9812509
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Adipocytes/drug effects/metabolism
MH  - Animals
MH  - Diabetes Mellitus, Type 2/*blood/complications/genetics
MH  - Dyslipidemias/*blood/complications/genetics
MH  - Female
MH  - *Lipolysis
MH  - *Models, Biological
MH  - Norepinephrine/pharmacology
MH  - Obesity/*blood/complications/genetics
MH  - Phenotype
MH  - Rats
MH  - Rats, Inbred SHR
EDAT- 2009/07/11 09:00
MHDA- 2009/07/30 09:00
CRDT- 2009/07/11 09:00
PHST- 2009/07/11 09:00 [entrez]
PHST- 2009/07/11 09:00 [pubmed]
PHST- 2009/07/30 09:00 [medline]
AID - 10.1007/BF03165967 [doi]
PST - ppublish
SO  - J Physiol Biochem. 2009 Mar;65(1):33-41. doi: 10.1007/BF03165967.