PMID- 29376304
OWN - NLM
STAT- MEDLINE
DCOM- 20180216
LR  - 20180216
IS  - 0042-8833 (Print)
IS  - 0042-8833 (Linking)
VI  - 85
IP  - 6
DP  - 2016
TI  - [Comparative characteristics of in vivo models of hyperlipidemia in Wistar rats 
      and C57Bl/6 mice].
PG  - 14-23
AB  - In vivo simulation of lipid disorders (hyperlipidemia, obesity, metabolic 
      syndrome, atherosclerosis) is of considerable interest to search for genomic, 
      transcriptomic and metabolomic markers that allow for differential diagnosis, 
      prognosis and selection of personalized diet therapy in patients with such 
      pathology. The aim of the study was the development and characterization of basic 
      biochemical parameters of in vivo models of alimentary hyperlipidemia in outbred 
      rats and inbred mice. The experiment was con-ducted on 48 growing female Wistar 
      rats, and 48 growing female mice of line C57Black/6, which were divided into 12 
      groups of 8 animals per group. Within 63 days the rats and mice of first 
      (control) group received a balanced semi synthetic diet (BD), the animals of the 
      second groups - high-fat diet (HFD) with 30% of the total fat by weight of dry 
      feed, third groups - BD and fructose solution (Fr) instead of water, the fourth 
      groups -HFD + Fr, fifth groups - BD supplemented with 0.5% cholesterol (Cho) by 
      weight of dry feed, sixth groups - BD with Cho and Fr. The amount and composition 
      of diets consumed were corrected during the experiment for their closest approach 
      in calories. After removal of animals from the experiment there were determined 
      the mass of internal organs, HDL, LDL, total cholesterol, triglycerides, glucose 
      in blood plasma, total lipids and their fatty acid composition in liver, ghrelin, 
      GIP, GLP-1, glucagon, leptin, PAI-1, resistin levels in blood plasma. It was 
      found that in both species the liver is the most sensitive to nutritional 
      imbalance, nutrient exerting the greatest impact on this was Fr. In rats, as 
      compared to mice, there was significantly more pronounced shifts in lipoprotein 
      spectrum in response to nutritional imbalances, especially to the consumption of 
      additional Cho, which was manifested in an increase of LDL, decrease of HDL and 
      magnification of atherogenic index. In the liver of rats fed diets with Cho, 
      marked steatosis developed manifested in a disproportionate increase in the lipid 
      content and accompanied by changes in their fatty acid composition, especially in 
      the ratio omega6 to omega3 PUFAs. Changing of hormones - regula-tors of carbohydrate 
      metabolism (GLP, glucagon) and ghrelin was significantly greater in mice than in 
      rats as a result of consumption of additional Fr. Effect had the opposite 
      direction in two species of Cho and Fr combining on leptin levels. The 
      significance is dis-cussed of the revealed interspecies differences in the light 
      of the characteristics of lipid and glucose metabolism in these two lines of 
      animals that are the most common models of alimentary-dependent diseases.
FAU - Apryatin, S A
AU  - Apryatin SA
FAU - Mzhelskaya, K V
AU  - Mzhelskaya KV
FAU - Trusov, N V
AU  - Trusov NV
FAU - Balakina, A S
AU  - Balakina AS
FAU - Kulakova, S N
AU  - Kulakova SN
FAU - Soto, S Kh
AU  - Soto SK
FAU - Makarenko, M A
AU  - Makarenko MA
FAU - Riger, N A
AU  - Riger NA
FAU - Tutelyan, V A
AU  - Tutelyan VA
LA  - rus
PT  - Comparative Study
PT  - Journal Article
PL  - Russia (Federation)
TA  - Vopr Pitan
JT  - Voprosy pitaniia
JID - 2984870R
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Dietary Fats)
RN  - 30237-26-4 (Fructose)
SB  - IM
MH  - Animals
MH  - Dietary Carbohydrates/*adverse effects/pharmacology
MH  - Dietary Fats/*adverse effects/pharmacology
MH  - *Disease Models, Animal
MH  - Female
MH  - Fructose/*adverse effects/pharmacology
MH  - *Hyperlipidemias/blood/chemically induced/pathology
MH  - Mice
MH  - Rats
MH  - Rats, Wistar
EDAT- 2016/01/01 00:00
MHDA- 2018/02/17 06:00
CRDT- 2018/01/30 06:00
PHST- 2016/01/01 00:00 [pubmed]
PHST- 2018/02/17 06:00 [medline]
PHST- 2018/01/30 06:00 [entrez]
PST - ppublish
SO  - Vopr Pitan. 2016;85(6):14-23.