Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach

Ahmed, Abeer; Balogun, Kayode; Bykova, Natalia V.; Cheema, Sukhinder Kaur

doi:10.1186/1743-7075-11-6

Cited by 33 publications

(28 citation statements)

References 90 publications

(93 reference statements)

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“…Furthermore, hepatic SMP30 protein levels in male Syrian golden hamsters were significantly downregulated in response to high‐fructose feeding (60% fructose) for 8 weeks . Recently, C57BL/6 female mice fed an omega‐3 polyunsaturated fatty acid‐rich diet showed lower protein levels of hepatic regucalcin (alternative name of SMP30) compared with mice fed less of the latter constituent despite the same fat content (20% fat) . These combined reports suggest that hepatic SMP30 expression is regulated according to an excessive dietary fat and nutritional composition, although clarification of the regulatory mechanism of SMP30 expression is still to come.…”

Section: Smp30 Knockout Leprdb/db Mice As a Novel Model Of Nashmentioning

confidence: 99%

Involvement of senescence marker protein‐30 in glucose metabolism disorder and non‐alcoholic fatty liver disease

Kondo

Ishigami

2016

Geriatrics Gerontology Int

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Senescence marker protein-30 (SMP30) was found to decrease in the liver, kidneys and lungs of mice during aging. SMP30 is a pleiotropic protein that acts to protect cells from apoptosis by enhancing plasma membrane Ca 2+ -pump activity and is bona fide gluconolactonase (EC 3.1.1.17) that participates in the penultimate step of the vitamin C biosynthetic pathway. For the past several years, we have obtained strong evidence showing the close relationship between SMP30, glucose metabolism disorder and non-alchoholic fatty liver disease in experiments with SMP30 knockout mice. Emerging proof links the following abnormalities: (i) the reduction of SMP30 by aging and/or excessive dietary fat or genetic deficiency causes a loss of Ca 2+ pumping activity, which impairs acute insulin release in pancreatic β-cells, initiates inflammatory responses with oxidative stress and endoplasmic reticulum stress in non-alchoholic steatohepatitis, exacerbates renal tubule damage, and introduces tubulointerstitial inflammation and fibrosis in diabetic nephropathy; (ii) vitamin C insufficiency also impairs acute insulin secretion in pancreatic β-cells by a mechanism distinct from that of the SMP30 deficiency; and (iii) the increased oxidative stress by concomitant deficiencies of SMP30, superoxide dismutase 1 and vitamin C similarly causes hepatic steatosis. Here, we review recent advances in our understanding of SMP30 in glucose metabolism disorder and non-alchoholic fatty liver disease. Geriatr Gerontol Int 2016; 16 (Suppl. 1): 4-16.Keywords: aging, diabetes mellitus, non-alchoholic fatty liver disease, senescence marker protein-30, vitamin C. Senescence marker protein-30 and its knockout miceSenescence marker protein-30 (SMP30) was first discovered in 1991 as an age-associated protein that decreased quantifiably in livers of aged rats.1,2 Thereafter, SMP30 proved to decrease in the liver, kidneys and lungs of mice during aging.3-5 Immunohistochemical analysis in the liver and primary cultured hepatocytes showed that SMP30 staining appeared in some, but not all, parenchymal cells, and localized in both the nuclei and cytoplasm.5 Furthermore, SMP30-positive cells localized mainly around the central veins in the livers of mice, and decreased numerically with aging.5 As established by reverse transcription polymerase chain reaction analysis, SMP30 transcripts were detected in not only the liver, kidneys and lungs of mice, but also in their brain, thymus, heart, testes and ovary; however, no SMP30 transcripts were identified in the spleen. 4,6 In humans, SMP30 was seen in parenchymal cells of the liver, proximal tubular cells of the kidney, acinal and ductal cells of the pancreas, and fasciculate cells of the adrenal cortex by applying immunohistochemical stain. 2,7 The human SMP30 gene is located in the p11.3-q11.2 segment of the X chromosome, 8 and its amino acid sequences are highly conserved among vertebrates. 7SMP30 knockout mice were established as a laboratory strain to clarify the physiological functions and the relationships bet...

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Section: Smp30 Knockout Leprdb/db Mice As a Novel Model Of Nashmentioning

confidence: 99%

Involvement of senescence marker protein‐30 in glucose metabolism disorder and non‐alcoholic fatty liver disease

Kondo

Ishigami

2016

Geriatrics Gerontology Int

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“…It has been generally accepted that an increase in omega-6 fatty acids may be detrimental to health, given the pathways some of which these fatty acids undergo when in excess (Ahmed, Balogun, Bykova, & Sukhinder, 2014;Roca Fernandez & Gonzalez Rodriguez, 2012). In this respect, from scientific evidence nutritionists have over the years urged for a decrease in this ratio.…”

Section: Fatty Acid Indices and Ratiosmentioning

confidence: 97%

Socio-economic dynamics and innovative technologies affecting health-related lipid content in diets: Implications on global food and nutrition security

Nantapo

Muchenje

Nkukwana

et al. 2015

Food Research International

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“…Too much inflammation will also result in damage, leading to apoptosis activation, necrosis and cell death [13]. Similar mechanism dealing with oxidative stress has been speculated to occur with the omega-3 fatty acid, C18:3n-3 (α-linolenic acid) and to a much greater effect by the long chain omega-3 fatty acids C20:5n-3 eicosapentaenoic acid (EPA) and C22:6n-3 docosahexaenoic acid (DHA) [14,15]. The oxidative effects of DHA are partially attenuated by co-treatment with the anti-oxidative vitamin E (α-tocopherol) [16].…”

Section: Introductionmentioning

confidence: 92%

CLA isomer t10,c12 induce oxidation and apoptosis in 3t3 adipocyte cells in a similar effect as omega-3 linolenic acid and DHA.

Meadus¹,

Vahmani²,

Duff³

et al. 2017

FFHD

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Citation: Meadus WJ, Vahmani P, Duff P, Zantinge JL, Turner TD, and Dugan M.E.R. Oxidation and apoptosis are induced by CLA-t10c12 similar to DHA in 3T3 adipocyte cells. Functional Foods in Health and Disease 2017; 7(2): 149-167 ABSTRACT Background: Commercial conjugated linoleic acid (CLA) dietary supplements contain an equal mixture of the C18:2 isomers, cis-9trans-11 and trans-10cis-12. Predominantly, CLAc9t11 occurs naturally in meat and dairy products at ~ 0.5% of total fat , whereas CLAt10c12 occurs at > 0.1%. Recent studies show that CLA-c9t11 generally promotes lipid accumulation but CLA-t10c12 may inhibit lipid accumulation and may also promote inflammation. The omega-3 fatty acids α-linolenic acid (C18:3n-3) and docosahexaenoic acid (DHA) have also been observed to inhibit lipid accumulation and effect inflammation; therefore we examined the effects of the two main isomers of CLA and omega -3 fatty acids C18:3n-3 and DHA at the molecular level to determine if they are causing similar oxidative stresses.Methods: Purified CLA-c9t11 and CLA-t10c12 were added to 3T3 cells induced into mature adipocyte cultures at 100uM concentrations and compared with 100uM C18:3n-3 (α-linolenic acid) and 50uM docosahexaenoic acid (DHA) to observe their effect on growth, gene transcription and general oxidation. The results of multiple separate trials were averaged and compared for significance at levels of P < 0.05, using one way ANOVA and Student's t-test.Results: C18:3n-3, DHA and CLA-t10c12 inhibited 3T3 adipose cell growth and caused a significant increase in lipid hydro peroxide activity. CLA-t10c12 and c9t11 increased AFABP, FAS and ACOX1 mRNA gene expression but DHA and C18:3n-3 decreased the same mRNAs. CLA-c9t11 but not the t10c12 stimulated adipoQ expression even though; CLA-c9t11 had only a slightly greater affinity for PPARγ than CLA-t10c12, according to TR-FRET assays. The expression of the xenobiotic metabolism genes, aldo-keto reductase 1c1 (akr1c1), superoxide dismutase (SOD) and inflammation chemokine secretions of eotaxin (CCL11), Rantes (CCL5), MIG (CCL9) and MCP-1 were increased by DHA, C18:3n-3 and CLA-t10c12 but not CLA-c9t11. This correlated with an increase in apoptosis factors, caspase 3, Bcl-2 and BAXs. Apoptosis factors were partially reduced by co-treatment with lipophilic anti-oxidant α-tocopherol.Conclusions: CLA-t10c12 stimulated the production of more reactive oxygen species (ROS) than CLA-c9t11. In response, cascades of genes are activated in detoxification, inflammation or apoptosis, to deal with the potentially damaging effects of ROS including CCL5 and MCP-1. This was similar to treatment with the omega-3 fatty acids but the fat metabolic enzymes were generally inhibited by C18:3n-3 and DHA except CLA-t10c12 which did not stimulate adipoQ.

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Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach

Cited by 33 publications

References 90 publications

Involvement of senescence marker protein‐30 in glucose metabolism disorder and non‐alcoholic fatty liver disease

Involvement of senescence marker protein‐30 in glucose metabolism disorder and non‐alcoholic fatty liver disease

Socio-economic dynamics and innovative technologies affecting health-related lipid content in diets: Implications on global food and nutrition security

CLA isomer t10,c12 induce oxidation and apoptosis in 3t3 adipocyte cells in a similar effect as omega-3 linolenic acid and DHA.

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