-
Something wrong with this record ?
Aspalathin alleviates skeletal muscle insulin resistance and mitochondrial dysfunction
SE. Mazibuko-Mbeje, SX. Mthembu, CJ. Muller, K. Ziqubu, N. Muvhulawa, RV. Modibedi, L. Tiano, PV. Dludla
Language English Country Czech Republic
Document type Journal Article
NLK
Directory of Open Access Journals
from 1991
Free Medical Journals
from 1998
PubMed Central
from 2020
ProQuest Central
from 2005-01-01
Medline Complete (EBSCOhost)
from 2006-01-01
Nursing & Allied Health Database (ProQuest)
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1998
- MeSH
- Diabetes Mellitus, Type 2 * metabolism MeSH
- Glucose metabolism MeSH
- Insulin pharmacology MeSH
- Insulin Resistance * physiology MeSH
- Muscle Fibers, Skeletal metabolism MeSH
- Muscle, Skeletal metabolism MeSH
- Humans MeSH
- Mitochondria metabolism MeSH
- Palmitates MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Natural compounds may bear promising therapeutic benefits against metabolic diseases such as type 2 diabetes mellitus (T2DM), which are characterized by a state of insulin resistance and mitochondrial dysfunction. Here, we examined the cellular mechanisms by which aspalathin, a dihydrochalcone C-glucoside unique to rooibos, may ameliorate palmitate-induced insulin resistance and mitochondrial dysfunction in cultured C2C12 myotubules. This current study demonstrated that aspalathin remains effective in improving glucose uptake in insulin-resistant skeletal muscle cells, supported by the upregulation of insulin-dependent signaling that involves the activation of insulin receptor (IR) and direct phosphorylation of protein kinase B (AKT). Interestingly, aspalathin also improved mitochondrial respiration and function, which was evident by an increased expression of carnitine palmitoyltransferase 1 (Cpt1), fatty acid transport protein 1 (Fatp1), sirtuin 1 (Sirt1), nuclear respiratory factor 1 (Nrf1), and transcription factor A, mitochondrial (Tfam). Importantly, our results showed that aspalathin treatment was effective in ameliorating the devastating outcomes of insulin resistance and mitochondrial dysfunction that are linked with an undesired pro-inflammatory response, by reducing the levels of well-known pro-inflammatory markers such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and protein kinase C-theta (PKC-theta). Thus, beyond improving glucose uptake and insulin signaling, the current study brings a new perspective in the therapeutic benefits of aspalathin in improving mitochondrial respiration and blocking inflammation to attenuate the detrimental effect of palmitate in skeletal muscle cells.
Department of Biochemistry and Microbiology University of Zululand KwaDlangezwa South Africa
Department of Biochemistry North West University Mafikeng Campus Mmabatho South Africa
Department of Life and Environmental Sciences Polytechnic University of Marche Ancona Italy
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22029560
- 003
- CZ-PrNML
- 005
- 20230518101830.0
- 007
- ta
- 008
- 230113s2022 xr ad f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.934844 $2 doi
- 035 __
- $a (PubMed)36047722
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Mazibuko-Mbeje, S. E. $u Department of Biochemistry, North-West University, Mafikeng Campus, Mmabatho, South Africa
- 245 10
- $a Aspalathin alleviates skeletal muscle insulin resistance and mitochondrial dysfunction / $c SE. Mazibuko-Mbeje, SX. Mthembu, CJ. Muller, K. Ziqubu, N. Muvhulawa, RV. Modibedi, L. Tiano, PV. Dludla
- 520 9_
- $a Natural compounds may bear promising therapeutic benefits against metabolic diseases such as type 2 diabetes mellitus (T2DM), which are characterized by a state of insulin resistance and mitochondrial dysfunction. Here, we examined the cellular mechanisms by which aspalathin, a dihydrochalcone C-glucoside unique to rooibos, may ameliorate palmitate-induced insulin resistance and mitochondrial dysfunction in cultured C2C12 myotubules. This current study demonstrated that aspalathin remains effective in improving glucose uptake in insulin-resistant skeletal muscle cells, supported by the upregulation of insulin-dependent signaling that involves the activation of insulin receptor (IR) and direct phosphorylation of protein kinase B (AKT). Interestingly, aspalathin also improved mitochondrial respiration and function, which was evident by an increased expression of carnitine palmitoyltransferase 1 (Cpt1), fatty acid transport protein 1 (Fatp1), sirtuin 1 (Sirt1), nuclear respiratory factor 1 (Nrf1), and transcription factor A, mitochondrial (Tfam). Importantly, our results showed that aspalathin treatment was effective in ameliorating the devastating outcomes of insulin resistance and mitochondrial dysfunction that are linked with an undesired pro-inflammatory response, by reducing the levels of well-known pro-inflammatory markers such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and protein kinase C-theta (PKC-theta). Thus, beyond improving glucose uptake and insulin signaling, the current study brings a new perspective in the therapeutic benefits of aspalathin in improving mitochondrial respiration and blocking inflammation to attenuate the detrimental effect of palmitate in skeletal muscle cells.
- 650 _2
- $a lidé $7 D006801
- 650 12
- $a inzulinová rezistence $x fyziologie $7 D007333
- 650 12
- $a diabetes mellitus 2. typu $x metabolismus $7 D003924
- 650 _2
- $a inzulin $x farmakologie $7 D007328
- 650 _2
- $a kosterní svaly $x metabolismus $7 D018482
- 650 _2
- $a kosterní svalová vlákna $x metabolismus $7 D018485
- 650 _2
- $a palmitany $7 D010168
- 650 _2
- $a glukosa $x metabolismus $7 D005947
- 650 _2
- $a mitochondrie $x metabolismus $7 D008928
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Mthembu, S. Xh. $u Department of Biochemistry, North-West University, Mafikeng Campus, Mmabatho, South Africa $u Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, South Africa
- 700 1_
- $a Muller, C. J. F. $u Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, South Africa $u Centre for Cardiometabolic Research Africa (CARMA), Division of Medical Physiology, Stellenbosch University, Tygerberg, South Africa $u Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa, South Africa
- 700 1_
- $a Ziqubu, K. $u Department of Biochemistry, North-West University, Mafikeng Campus, Mmabatho, South Africa
- 700 1_
- $a Muvhulawa, N. $u Department of Biochemistry, North-West University, Mafikeng Campus, Mmabatho, South Africa
- 700 1_
- $a Modibedi, R. V. $u Department of Biochemistry, North-West University, Mafikeng Campus, Mmabatho, South Africa
- 700 1_
- $a Tiano, L. $u Department of Life and Environmental Sciences, Polytechnic University of Marche, Ancona, Italy
- 700 1_
- $a Dludla, P. V. $u Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, South Africa
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 71, č. 5 (2022), s. 643-656
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/36047722 $y Pubmed
- 910 __
- $a ABA008 $b A 4120 $c 266 $y p $z 0
- 990 __
- $a 20230113 $b ABA008
- 991 __
- $a 20230518101824 $b ABA008
- 999 __
- $a ok $b bmc $g 1894755 $s 1180885
- BAS __
- $a 3
- BAS __
- $a PreBMC-MEDLINE
- BMC __
- $a 2022 $b 71 $c 5 $d 643-656 $e 20220831 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- LZP __
- $b NLK198 $a Pubmed-20230113
