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Probiotic Lactobacillus casei Zhang ameliorates high-fructose-induced impaired glucose tolerance in hyperinsulinemia rats.

AbstractAIM:
To evaluate the preventive and therapeutic effects of Lactobacilluscasei Zhang on impaired glucose tolerance (IGT) by using fructose-induced hyperinsulinemia rats.
METHODS:
Rats were fed 25 % fructose solution for hyperinsulinemia with L.casei Zhang for prevention or therapy. Serum levels of insulin, glucagon-like peptide-2 (GLP-2), osteocalcin, malondialdehyde (MDA), total intestinal bile acids and hepatic glycogen contents were determined by assay kits. The major bacteria from feces and liver expression of adiponectin receptor 2 (AdipoR2), liver X receptor-α (LXR-α), peroxisome proliferator-activated receptor gamma (PPAR-γ) and vitamin K epoxide reductase complex subunit 1 mRNA were assessed by RT-PCR. Pancreas injury was evaluated by histological analysis.
RESULTS:
Lactobacilluscasei Zhang significantly increased numbers of Lactobacillus and Bifidobacterium and decreased Clostridium in the intestine (p < 0.01). Meanwhile, liver glycogen contents were significantly decreased (p < 0.05). In preventive group, accompanied by significantly lower insulin and GLP-2 levels (p < 0.05), L.casei Zhang prevented rats from an increase in oral glucose tolerance area under curve (AUC) which was significant in hyperinsulinemia group (p < 0.05). In therapeutic group, L.casei Zhang administration possessed improved glucose tolerance (p < 0.05), which were associated with increased osteocalcin level (p < 0.01), improved intestinal bile acids secretion (p = 0.060), decreased serum MDA levels (p < 0.05) and upregulation of LXR-α, PPAR-γ and AdipoR2 gene expression, as well as an increase in Bacteroides fragilis (p < 0.05).
CONCLUSIONS:
Lactobacilluscasei Zhang administration exert both preventive and ameliorative effect on oral glucose tolerance AUC in IGT rats but may be via different mechanisms. L.casei Zhang could prevent rats from increased AUC through GLP-2 lowering, while the ameliorative effect in high-fructose-fed post-adolescent rats may be via B. fragilis enriched vitamin K2-dependent osteocalcin mechanism in which AdipoR2, LXR-α and PPAR-γ signaling were involved.
AuthorsYong Zhang, Lifeng Wang, Jiachao Zhang, Yunxu Li, Qiuwen He, He Li, Xiao Guo, Jianlin Guo, Heping Zhang
JournalEuropean journal of nutrition (Eur J Nutr) Vol. 53 Issue 1 Pg. 221-32 (Feb 2014) ISSN: 1436-6215 [Electronic] Germany
PMID23797890 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Glucagon-Like Peptide 2
  • Insulin
  • Liver X Receptors
  • Nr1h3 protein, rat
  • Orphan Nuclear Receptors
  • PPAR gamma
  • RNA, Messenger
  • Receptors, Adiponectin
  • adiponectin receptor 2, rat
  • Osteocalcin
  • Fructose
  • Malondialdehyde
  • Vitamin K Epoxide Reductases
Topics
  • Animals
  • Area Under Curve
  • Bifidobacterium (isolation & purification)
  • Clostridium (isolation & purification)
  • Fructose (administration & dosage, adverse effects)
  • Glucagon-Like Peptide 2 (blood)
  • Glucose Intolerance (chemically induced, diet therapy)
  • Glucose Tolerance Test
  • Hyperinsulinism (chemically induced, diet therapy)
  • Insulin (blood)
  • Intestinal Mucosa (metabolism)
  • Intestines (microbiology)
  • Lactobacillus (isolation & purification)
  • Lacticaseibacillus casei
  • Liver X Receptors
  • Male
  • Malondialdehyde (blood)
  • Orphan Nuclear Receptors (metabolism)
  • Osteocalcin (blood)
  • PPAR gamma (metabolism)
  • Probiotics (administration & dosage)
  • RNA, Messenger (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adiponectin (metabolism)
  • Up-Regulation
  • Vitamin K Epoxide Reductases (metabolism)

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