Key result
UCP2 deficiency improved blood glucose and insulin sensitivity in high-fat diet-fed mice, associated with significant upregulation of genes in the PPAR signaling pathway (P=3.19x10^-11).
Why the study?
Does UCP2 deficiency improve glucose and lipid metabolism and insulin sensitivity in high-fat diet-fed mice?
RCT
randomly assigned
Does UCP2 deficiency improve glucose and lipid metabolism and insulin sensitivity in high-fat diet-fed mice?
p-value: p=3.19 × 10(-11)
UCP2 deficiency improves glucose and lipid metabolism and insulin sensitivity in mice on a high-fat diet, likely mediated by upregulation of the PPAR signaling pathway.
AIMS/INTRODUCTION: Uncoupling protein 2 (UCP2), which was an important mitochondrial inner membrane protein associated with glucose and lipid metabolism, widely expresses in all kinds of tissues including hepatocytes. The present study aimed to explore the impact of UCP2 deficiency on glucose and lipid metabolism, insulin sensitivity and its effect on the liver-associated signaling pathway by expression profiling analysis. MATERIALS AND METHODS: Four-week-old male UCP2-/- mice and UCP2+/+ mice were randomly assigned to four groups: UCP2-/- on a high-fat diet, UCP2-/- on a normal chow diet, UCP2+/+ on a high-fat diet and UCP2+/+ on a normal chow diet. The differentially expressed genes in the four groups on the 16th week were identified by Affymetrix gene array. RESULTS: The results of intraperitoneal glucose tolerance test and insulin tolerance showed that blood glucose and β-cell function were improved in the UCP2-/- group on high-fat diet. Enhanced insulin sensitivity was observed in the UCP2-/- group. The differentially expressed genes were mapped to 23 pathways (P < 0.05). We concentrated on the 'peroxisome proliferator-activated receptor (PPAR) signaling pathway' (P = 3.19 × 10(-11)), because it is closely associated with the regulation of glucose and lipid profiles. In the PPAR signaling pathway, seven genes (PPARγ, Dbi, Acsl3, Lpl, Me1, Scd1, Fads2) in the UCP2-/- mice were significantly upregulated. CONCLUSIONS: The present study used gene arrays to show that activity of the PPAR signaling pathway involved in the improvement of glucose and lipid metabolism in the liver of UCP2-deficient mice on a long-term high-fat diet. The upregulation of genes in the PPAR signaling pathway could explain our finding that UCP2 deficiency ameliorated insulin sensitivity. The manipulation of UCP2 protein expression could represent a new strategy for the prevention and treatment of diabetes.
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Zhou et al. (2015) conducted an RCT in Diabetes and metabolic dysfunction. UCP2 deficiency (UCP2-/-) vs. Wild-type (UCP2+/+) was evaluated on Differentially expressed genes mapped to the PPAR signaling pathway (p=3.19 × 10(-11)). UCP2 deficiency improved blood glucose and insulin sensitivity in high-fat diet-fed mice, associated with significant upregulation of genes in the PPAR signaling pathway (P=3.19x10^-11).
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