Skip to content
Licensed Unlicensed Requires Authentication Published by De Gruyter August 15, 2019

Effect of crude Moringa oleifera Lam. seed extract on the blood markers of metabolic syndrome in high-fructose diet-fed growing Sprague-Dawley rats

  • Masiline Mapfumo , Busisani W. Lembede ORCID logo EMAIL logo , Ashwell R. Ndhlala and Eliton Chivandi

Abstract

Background

Moringa oleifera seed has anti-diabetic and anti-obesogenic properties. This study interrogated the effect of crude hydroethanolic M. oleifera seed extract on the blood markers of metabolic syndrome (MetS) in high-fructose diet fed growing Sprague-Dawley rats.

Methods

Sixty 21-day old female and male Sprague-Dawley rat pups were randomly allocated to and administered one of the following treatment regimens daily for twelve weeks: group I – plain drinking water (PW)+plain gelatine cube (PC), group II – 20% (w/v) fructose solution (FS)+PC, group III – FS+100 mg/kg body mass fenofibrate in gelatine cube (FN), group IV – FS+low dose (50 mg/kg body mass) of M. oleifera in gelatine cube (LMol) and group V – FS+high dose (500 mg/kg body mass) of M. oleifera in gelatine cube (HMol). The rats in each treatment regimen had ad libitum access to a standard rat chow. After the 12-week trial, the rats were subjected to an oral glucose tolerance test and then euthanised 48 h later. Blood was collected. Plasma triglyceride, cholesterol and insulin concentration were determined. HOMA-IR was then computed.

Results

The high-fructose diet increased (p<0.05) plasma insulin concentration and HOMA-IR in female rats only. It increased plasma triglyceride concentration in both female and male rats and plasma cholesterol concentration in male rats only. The crude hydroethanolic M. oleifera seed extract prevented the high-fructose diet-induced metabolic derangements in male and female rats.

Conclusion

Crude hydroethanolic M. oleifera seed extract can potentially be used as a prophylactic intervention for diet-induced MetS in children.

Abbreviations

ARC – VOP

Agricultural Research Council’s Vegetable and Ornamental Plants

AUC

area under the curve

FS

20% (w/v) fructose solution

FN

100 mg/kg body mass fenofibrate

HFD

high-fructose diet

HOMA-IR

homeostatic model assessment of insulin resistance

HMol

500 mg/kg M. oleifera seed extract

LMol

50 mg/kg body mass M. oleifera seed extract

MetS

metabolic syndrome

OGTT

oral glucose tolerance test

PC

plain gelatine cube

PW

plain water

Acknowledgments

We would like to express our gratitude to Professor Kennedy H. Erlwanger, Ms Monica Gomes, the postgraduate colleagues from Endocrinology, Metabolism and Nutrition Research laboratory and the CAS staff for their technical support. The Faculty of Health Sciences Research Office, University of the Witwatersrand and the National Research Foundation (SA) are acknowledged for financially supporting this study.

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

  6. Declaration of interest: none.

References

[1] Saklayen MG. The global epidemic of the metabolic syndrome. Curr Hypertens Rep 2018;20:12.10.1007/s11906-018-0812-zSearch in Google Scholar

[2] Nolan PB, Carrick-Ranson G, Stinear JW, Reading SA, Dalleck LC. Prevalence of metabolic syndrome and metabolic syndrome components in young adults: a pooled analysis. Prev Med Reports 2017;7:211–15.10.1016/j.pmedr.2017.07.004Search in Google Scholar

[3] Rivera DS, Lindsay CB, Codocedo JF, Carreño LE, Cabrera D, Arrese MA, et al. Long-term, fructose-induced metabolic syndrome-like condition is associated with higher metabolism, reduced synaptic plasticity and cognitive impairment in Octodon degus. Mol Neurobiol 2018;55:9169–87.10.1007/s12035-018-0969-0Search in Google Scholar

[4] Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev 2010;90:23–46.10.1152/physrev.00019.2009Search in Google Scholar

[5] Rutledge AC, Adeli K. Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms. Nutr Rev 2008;65:S13–23.10.1111/j.1753-4887.2007.tb00322.xSearch in Google Scholar

[6] Dekker MJ, Su Q, Baker C, Rutledge AC, Adeli K. Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome. Am J Physiol Endocrinol Metab 2010;299:E685–94.10.1152/ajpendo.00283.2010Search in Google Scholar

[7] Basciano H, Federico L, Adeli K. Fructose, insulin resistance, and metabolic dyslipidemia. Nutr Metab (Lond) 2005;2:5.10.1186/1743-7075-2-5Search in Google Scholar

[8] Al-Mahmood A, Afrin S, Hoque N. Dyslipidemia in insulin resistance: cause or effect. Bangladesh J Med Biochem 2014;7:27–31.10.3329/bjmb.v7i1.18576Search in Google Scholar

[9] Grundy SM. Hypertriglyceridemia, insulin resistance, and the metabolic syndrome. Am J Cardiol 1999;83:25F–9F.10.1016/S0002-9149(99)00211-8Search in Google Scholar

[10] Li N, Fu J, Koonen DP, Kuivenhoven JA, Snieder H, Hofker MH. Are hypertriglyceridemia and low HDL causal factors in the development of insulin resistance?. Atherosclerosis 2014;233:130–8.10.1016/j.atherosclerosis.2013.12.013Search in Google Scholar PubMed

[11] Ooi EM, Ng TW, Watts GF, Chan DC, Barrett PH. Effect of fenofibrate and atorvastatin on VLDL apoE metabolism in men with the metabolic syndrome. J Lipid Res 2012;53:2443–9.10.1194/jlr.P029223Search in Google Scholar

[12] Fyhrquist P, Mwasumbi L, Hæggström CA, Vuorela HI, Hiltunen R, Vuorela P. Ethnobotanical and antimicrobial investigation on some species of Terminalia and Combretum (Combretaceae) growing in Tanzania. J Ethnopharmacol 2002;79:169–77.10.1016/S0378-8741(01)00375-0Search in Google Scholar

[13] Fahey JW. Moringa oleifera: a review of the medical evidence for its nutritional, therapeutic, and prophylactic properties. Part 1. Trees Life J 2005;1:1–15.Search in Google Scholar

[14] Leone A, Spada A, Battezzati A, Schiraldi A, Aristil J, Bertoli S. Moringa oleifera seeds and oil: characteristics and uses for human health. Int J Mol Sci 2016;17:E2141.10.3390/ijms17122141Search in Google Scholar PubMed PubMed Central

[15] Pandey A, Pandey R, Tripathi P, Gupta PP, Haider J, Bhatt S, et al. Moringa Oleifera Lam. Sahijan)-A plant with a plethora of diverse therapeutic benefits: an updated retrospection. Med Aromat Plants 2012;1:1–8.10.4172/2167-0412.1000101Search in Google Scholar

[16] Bais S, Singh GS, Sharma R. Antiobesity and hypolipidemic activity of Moringa oleifera leaves against high fat diet-induced obesity in rats. Adv Biol 2014;2014:1–9.10.1155/2014/162914Search in Google Scholar

[17] Mbikay M. Therapeutic potential of Moringa oleifera leaves in chronic hyperglycemia and dyslipidemia: a review. Front Pharmacol 2012;3:24.10.3389/fphar.2012.00024Search in Google Scholar PubMed PubMed Central

[18] Ajibola M, Eunice O, Stephanie IN. Effects of aqueous extract of Moringa oleifera seeds on alloxan induced hyperglycemia. Basic Sci Med 2014;3:37–42.Search in Google Scholar

[19] Al-Malki AL, El Rabey HA. The antidiabetic effect of low doses of Moringa oleifera Lam. seeds on streptozotocin induced diabetes and diabetic nephropathy in male rats. Biomed Res Int 2015;2015:381040.10.1155/2015/381040Search in Google Scholar PubMed PubMed Central

[20] Hamza AA. Ameliorative effects of Moringa oleifera Lam seed extract on liver fibrosis in rats. Food Chem Toxicol 2010;48:345–55.10.1016/j.fct.2009.10.022Search in Google Scholar PubMed

[21] Ajibade TO, Arowolo R, Olayemi FO. Phytochemical screening and toxicity studies on the methanol extract of the seeds of moringa oleifera. J Complement Integr Med 2013;10:1–6.10.1515/jcim-2012-0015Search in Google Scholar PubMed

[22] Fawole OA, Ndhlala AR, Amoo SO, Finnie JF, Van Staden J. Anti-inflammatory and phytochemical properties of twelve medicinal plants used for treating gastro-intestinal ailments in South Africa. J Ethnopharmacol 2009;123:237–43.10.1016/j.jep.2009.03.012Search in Google Scholar PubMed

[23] Kamerman PR, Modisa BM, Mphahlele NR. Atorvastatin, a potent HMG-CoA reductase inhibitor, is not antipyretic in rats. J Therm Biol 2004;29:431–5.10.1016/j.jtherbio.2004.08.012Search in Google Scholar

[24] Ferreira AV, Parreira GG, Porto LC, Mario ÉG, Delpuerto HL, Martins AS, et al. Fenofibrate prevents orotic acid–induced hepatic steatosis in rats. Life Sci 2008;82:876–83.10.1016/j.lfs.2008.02.003Search in Google Scholar PubMed

[25] Loxham SJ, Teague J, Poucher SM, De Schoolmeester J, Turnbull AV, Carey F. Glucagon challenge in the rat: a robust method for the in vivo assessment of Glycogen phosphorlyase inhibitor efficacy. J Pharmacol Toxicol Methods 2007;55:71–7.10.1016/j.vascn.2006.03.005Search in Google Scholar PubMed

[26] Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412–19.10.1007/BF00280883Search in Google Scholar PubMed

[27] Randriamboavonjy JI, Loirand G, Vaillant N, Lauzier B, Derbré S, Michalet S, et al. Cardiac protective effects of Moringa oleifera seeds in spontaneous hypertensive rats. Am J Hypertens 2016;29:873–81.10.1093/ajh/hpw001Search in Google Scholar PubMed

[28] Dias S, Paredes S, Ribeiro L. Drugs involved in dyslipidemia and obesity treatment: focus on adipose tissue. Int J Endocrinol 2018;2018:2637418.10.1155/2018/2637418Search in Google Scholar PubMed PubMed Central

[29] Ferreira AV, Parreira GG, Green A, Botion LM. Effects of fenofibrate on lipid metabolism in adipose tissue of rats. Metabolism 2006;55:731–5.10.1016/j.metabol.2006.01.020Search in Google Scholar PubMed

[30] Liu S, Liu Q, Li LY, Huan Y, Sun SJ, Shen ZF. Long-term fenofibrate treatment impaired glucose-stimulated insulin secretion and up-regulated pancreatic NF-kappa B and iNOS expression in monosodium glutamate-induced obese rats: is that a latent disadvantage?. J Transl Med 2011;9:176.10.1186/1479-5876-9-176Search in Google Scholar PubMed PubMed Central

Received: 2019-02-16
Accepted: 2019-04-01
Published Online: 2019-08-15

© 2019 Walter de Gruyter GmbH, Berlin/Boston

Downloaded on 22.3.2023 from https://www.degruyter.com/document/doi/10.1515/jcim-2019-0045/html
Scroll Up Arrow