PMID- 19855071
OWN - NLM
STAT- MEDLINE
DCOM- 20091110
LR  - 20131121
IS  - 1535-3699 (Electronic)
IS  - 1535-3699 (Linking)
VI  - 234
IP  - 11
DP  - 2009 Nov
TI  - High fat and highly thermolyzed fat diets promote insulin resistance and increase 
      DNA damage in rats.
PG  - 1296-304
LID - 10.3181/0904-RM-126 [doi]
AB  - Many studies have demonstrated that DNA damage may be associated with type 2 
      diabetes mellitus (T2DM) and its complications. The goal of this study was to 
      evaluate the effects of the potential relationship between fat (thermolyzed) 
      intake, glucose dyshomeostasis and DNA injury in rats. Biochemical parameters 
      related to glucose metabolism (i.e., blood glucose levels, insulin tolerance 
      tests, glucose tolerance tests and fat cell glucose oxidation) and general health 
      parameters (i.e., body weight, retroperitoneal and epididymal adipose tissue) 
      were evaluated in rats after a 12-month treatment with either a high fat or a 
      high thermolyzed fat diet. The high fat diet (HFD) and high fat thermolyzed diet 
      (HFTD) showed increased body weight and impaired insulin sensitivity at the 
      studied time-points in insulin tolerance test (ITT) and glucose tolerance test 
      (GTT). Interestingly, only animals subjected to the HFTD diet showed decreased 
      epididymal fat cell glucose oxidation. We show which high fat diets have the 
      capacity to reduce glycogen synthesis by direct and indirect pathways. HFTD 
      promoted an increase in lipid peroxidation in the liver, demonstrating 
      significant damage in lipids in relation to other groups. Blood and hippocampus 
      DNA damage was significantly higher in animals subjected to HFDs, and the highest 
      damage was observed in animals from the HFTD group. Striatum DNA damage was 
      significantly higher in animals subjected to HFDs, compared with the control 
      group. These results show a positive correlation between high fat diet, glucose 
      dyshomeostasis, oxidative stress and DNA damage.
FAU - de Assis, Adriano M
AU  - de Assis AM
AD  - Departamento de Bioquimica, Instituto de Ciencias Basicas da Saude, Universidade 
      Federal do Rio Grande do Sul, 90035-003, Porto Alegre, RS, Brazil
FAU - Rieger, Debora K
AU  - Rieger DK
FAU - Longoni, Aline
AU  - Longoni A
FAU - Battu, Cintia
AU  - Battu C
FAU - Raymundi, Suzeli
AU  - Raymundi S
FAU - da Rocha, Ricardo F
AU  - da Rocha RF
FAU - Andreazza, Ana C
AU  - Andreazza AC
FAU - Farina, Marcelo
AU  - Farina M
FAU - Rotta, Liane N
AU  - Rotta LN
FAU - Gottfried, Carmen
AU  - Gottfried C
FAU - Goncalves, Carlos A
AU  - Goncalves CA
FAU - Moreira, Jose Claudio
AU  - Moreira JC
FAU - Perry, Marcos L S
AU  - Perry ML
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Exp Biol Med (Maywood)
JT  - Experimental biology and medicine (Maywood, N.J.)
JID - 100973463
RN  - 0 (Dietary Fats)
RN  - 9005-79-2 (Glycogen)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adipose Tissue/drug effects/metabolism
MH  - Animals
MH  - *DNA Damage
MH  - Dietary Fats/administration & dosage/*pharmacology
MH  - Glucose/metabolism
MH  - Glucose Tolerance Test
MH  - Glycogen/biosynthesis
MH  - Hippocampus/drug effects/metabolism
MH  - *Insulin Resistance
MH  - Lipid Peroxidation/drug effects
MH  - Liver/drug effects/metabolism
MH  - Male
MH  - Neostriatum/drug effects/metabolism
MH  - Oxidation-Reduction/drug effects
MH  - Protein Carbonylation/drug effects
MH  - Rats
MH  - Rats, Wistar
MH  - *Temperature
EDAT- 2009/10/27 06:00
MHDA- 2009/11/11 06:00
CRDT- 2009/10/27 06:00
PHST- 2009/10/27 06:00 [entrez]
PHST- 2009/10/27 06:00 [pubmed]
PHST- 2009/11/11 06:00 [medline]
AID - 234/11/1296 [pii]
AID - 10.3181/0904-RM-126 [doi]
PST - ppublish
SO  - Exp Biol Med (Maywood). 2009 Nov;234(11):1296-304. doi: 10.3181/0904-RM-126.