Abstract | BACKGROUND: METHODS:
Antioxidant genes Sod2 (mitochondrial) and catalase (cytosolic) or null (control) were upregulated in human adipose tissue-derived MSCs using adenoviral constructs. Modified MSCs were then delivered intraperitoneally into mice that were fed a 45% or 60% high-fat diet (HFD), and animals were followed for 4 weeks. RESULTS: Over 4 weeks, body weight remained stable; however, we noted a significant reduction in liver fat content by histological analysis and liver triglyceride assay. Triglyceride assay (p < 0.01) confirmed reduced liver fat accumulation in animals that received either Sod2- or Cat-MSCs. There was a lower plasma level of inflammatory marker TNFα, measured in mice that were fed either 45% or 60% HFD and received Sod2- or Cat-MSCs, indicating reduced systemic inflammation. Ucp1 mRNA was upregulated approximately 100-1000-fold for omental fat and 10-100-fold for pericardial fat compared to the Null-MSC-receiving group. Pcgc1a and Prdm16 mRNA upregulation was also noted particularly for pericardial fat. Glucose tolerance showed a positive improvement trend with a lower area under the curve (AUC) values for both Sod2- and Cat-MSCs groups in comparison to control. For mice fed with 60% HFD and that received Sod2-MSCs, glucose levels were significantly lower than control (*p < 0.05) at a time point of 60 min in the glycemic curve during glucose tolerance test. CONCLUSION:
|
Authors | Cleyton C Domingues, Nabanita Kundu, Yana Kropotova, Neeki Ahmadi, Sabyasachi Sen |
Journal | Stem cell research & therapy
(Stem Cell Res Ther)
Vol. 10
Issue 1
Pg. 280
(09 02 2019)
ISSN: 1757-6512 [Electronic] England |
PMID | 31477174
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Antioxidants
- Blood Glucose
- RNA, Messenger
- Tumor Necrosis Factor-alpha
- Uncoupling Protein 1
- Superoxide Dismutase
- superoxide dismutase 2
|
Topics |
- Adiposity
(physiology)
- Animals
- Antioxidants
(metabolism)
- Blood Glucose
(metabolism)
- Cells, Cultured
- Diet, High-Fat
(adverse effects)
- Fatty Liver
(metabolism, pathology)
- Glucose Tolerance Test
(methods)
- Humans
- Inflammation
(metabolism, pathology)
- Liver
(metabolism, pathology)
- Male
- Mesenchymal Stem Cells
(metabolism, pathology)
- Mice
- Mice, Inbred C57BL
- Mice, Obese
- Obesity
(metabolism, pathology)
- Oxidative Stress
(physiology)
- RNA, Messenger
(metabolism)
- Superoxide Dismutase
(metabolism)
- Tumor Necrosis Factor-alpha
(metabolism)
- Uncoupling Protein 1
(metabolism)
- Up-Regulation
(physiology)
|