{"id":2409,"date":"2015-04-25T06:50:41","date_gmt":"2015-04-25T06:50:41","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=2409"},"modified":"2016-11-30T12:21:28","modified_gmt":"2016-11-30T12:21:28","slug":"amounts-of-hepatic-glucose-and-lipids-induced-by-honey-feeding-in-wistar-rats","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol5no1\/amounts-of-hepatic-glucose-and-lipids-induced-by-honey-feeding-in-wistar-rats\/","title":{"rendered":"Amounts of Hepatic Glucose and Lipids Induced by Honey Feeding in Wistar Rats"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

Honey is a popular viscous sweetener and a common household product used throughout the World.\u00a0 Popularity comes not only in being a natural sweetener but also because of its several proven or unproven benefits\u00a0 (Bansal, et al<\/em>., 2005).\u00a0 Honey is a natural substance produced by honey bees, Apis mellifera<\/em>, from the nectar of blossom or from exuduates of trees and plants.<\/p>\n

The composition of honey is rather variable and primarily depends on the floral source.\u00a0 Honey contains at least 181 substances (Chow, 2002).\u00a0 It is a super saturated solution of sugars, mainly composed of fructose (38%) and glucose (31%).\u00a0 It also contains minerals, proteins, free amino acids, enzymes and\u00a0 vitamins (Perez, 2002).<\/p>\n

The physiological and health effects of honey have been related to its antibacterial activity (Bogdanor, 1997), antioxidant capacity (Gheldof, et al<\/em>., 2003), antimutagenic, antitumour and anti-inflammatory activity (Molan, 2001), gastroenterology and cardiovascular effects.\u00a0 Yaghobi, et al<\/em>. (2008), reported that honey ameliorates cardiovascular risk factors in healthy individuals and in patients with elevated risk factors.\u00a0 Yoghoobi, et al<\/em>. (2008) and Al-Waili (2004) have reported the effects of honey on total cholesterol, low density cholesterol (LDL-C), high density cholesterol (HDL-C), triacylglycerol (TAG), fasting blood glucose and C-reactive protein (CRP).\u00a0 Busserolles, et al<\/em>. (2002), reported that substitution of honey for refined carbohydrates protects rats from hypertriglyceridemic and prooxidative effects of fructose. Munstedt, et al. (2009) also observed similar effect of honey on serum cholesterol and lipid values.\u00a0 However, this study compares the amounts of glucose and lipids in the livers of rats fed with honey and fructose.<\/p>\n

Materials and Methods<\/strong><\/p>\n

Experimental animals<\/strong><\/p>\n

Both male and female Wistar rats weighing between 60g-110g and obtained from the Animals House, Faculty of Basic Medical Sciences, Delta State University, Abraka, Nigeria, were used for the experiment.\u00a0 They were fed on growers\u2019 mash purchased from Top Feeds, Sapele, Delta State, and given water ad libitum<\/em>.\u00a0 The animals were housed in metal cages under controlled condition of 12 hours light\/12 hours dark cycle.<\/p>\n

Experiment design<\/strong><\/p>\n

A total of 49 rats were used for the experiment.\u00a0 The rats were fed growers\u2019 mash that was\u00a0 either sugar free or contained 20%, 30%, 40% honey or mixed sugar (fructose and glucose) equivalent to that in 20%, 30% and 40% honey for four weeks.\u00a0 The rats were divided into 7 groups of 7 rats per groups.<\/p>\n

Preparation of liver tissue homogenate<\/strong><\/p>\n

At the completion of the 4 \u2013 week feeding period, the rats were fasted overnight, sacrificed under anaesthesia (chloroform) and their livers were excised and collected for biochemical analysis.\u00a0 One gramme (1g) of wet liver tissue was homogenized in 9.0ml of normal saline.\u00a0 The supernatant obtained after centrifuging was\u00a0 kept frozen until required for assay which was performed within 72 h.<\/p>\n

Biochemical Assays<\/strong><\/p>\n

The amount of hepatic triacyglycerol was determined by the Trinder reaction (McGowan, et al<\/em>., 1983).\u00a0 Liver total cholesterol and HDL-cholesterol levels were\u00a0 estimated colorimetrically by the methods of Beaumont et al<\/em>. (1972) and Castelli et al<\/em>. (1977), respectively.\u00a0 Hepatic LDL-cholesterol content was calculated by the Friedewald formula (Wang, et al<\/em>., 1996).\u00a0 The concentration of liver glucose was assessed by the glucose oxidase method (Trinder, 1969).<\/p>\n

All\u00a0 the reagent test kits used for these assays were\u00a0 purchased from TECO Diagnostics, Anheim CA, USA.<\/p>\n

Statistics<\/strong><\/p>\n

All data were analyzed using ANOVA and group means were compared by Duncan\u2019s multiple range.\u00a0 Value of p<\/em><0.05 were considered significant.<\/p>\n

Results<\/strong><\/p>\n

The biochemical parameters measured which include liver glucose, liver triacylglycerol, total cholesterol, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) are shown in Tables 1 and 2 respectively.<\/p>\n

Table 1: Liver levels of glucose, triacylglycerol and total cholesterol in control and\u00a0experimental rats.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n
Groups<\/strong><\/td>\nGlucose (mmol\/L)<\/strong><\/td>\nTAG (mmol\/L)<\/strong><\/td>\nTotal<\/strong><\/td>\n<\/tr>\n
A<\/td>\n0.84\u00b10.16<\/td>\n0.62\u00b10.04<\/td>\n5.73\u00b10.56<\/td>\n<\/tr>\n
B<\/td>\n1.23\u00b10.28<\/td>\n0.68\u00b10.03<\/td>\n5.90\u00b10.24<\/td>\n<\/tr>\n
C<\/td>\n1.97\u00b10.44<\/td>\n0.73\u00b10.02<\/td>\n6.71\u00b10.54<\/td>\n<\/tr>\n
D<\/td>\n1.54\u00b10.09<\/td>\n0.78\u00b10.05<\/td>\n6.71\u00b10.37<\/td>\n<\/tr>\n
E<\/td>\n2.18\u00b10.31<\/td>\n0.74\u00b10.05<\/td>\n7.05\u00b10.46<\/td>\n<\/tr>\n
F<\/td>\n1.86\u00b10.12<\/td>\n0.78\u00b10.06<\/td>\n7.08\u00b10.64<\/td>\n<\/tr>\n
G<\/td>\n1.85\u00b10.28<\/td>\n0.83\u00b10.07<\/td>\n7.09\u00b10.37<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Values are expressed as mean \u00b1 SD for n=7 rats\/groups <\/em><\/p>\n

Group 1: Treated as control (100% feed) <\/em><\/p>\n

Group 2: Treated with 20% honey, 80% feed <\/em><\/p>\n

Group 3: Treated with 30% honey, 70% feed <\/em><\/p>\n

Group 4: Treated 40% honey, 60 feed <\/em><\/p>\n

Group 5: Treated with fructose\/glucose equivalent to amounts in 20% honey<\/em><\/p>\n

Group 6; Treated with fructose\/glucose equivalent to amounts in 30% honey. <\/em><\/p>\n

Group 7: Treated\u00a0 with fructose\/glucose equivalent to amounts in 40% honey. <\/em><\/p>\n

The results in Table 1, indicate that there were significant decreases (p<\/em><0.05) in the hepatic glucose, triacylglycerol and total cholesterol concentrations in rats fed with 100% feed (control) compared with the other six experimental groups.<\/p>\n

Table 2: Changes in hepatic HDL and LDL-cholesterol levels in control and experimental rats<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n
Groups<\/strong><\/td>\nHDL Cholesterol\u00a0 (mmol\/L)<\/strong><\/td>\nLDL-Cholesterol (mmol\/L)<\/strong><\/td>\n<\/tr>\n
A (100% Feed)<\/td>\n4.82\u00b10.35<\/td>\n0.63\u00b10.04<\/td>\n<\/tr>\n
B (20% Honey )<\/td>\n4.93\u00b10.24<\/td>\n0.66\u00b10.05<\/td>\n<\/tr>\n
C (30% Honey )<\/td>\n5.45\u00b10.43<\/td>\n0.09\u00b10.08<\/td>\n<\/tr>\n
D (40%) Honey )<\/td>\n5.48\u00b10.28<\/td>\n0.95\u00b10.07<\/td>\n<\/tr>\n
E(Fructose\/Glucose 20%)<\/td>\n4.82\u00b10.46<\/td>\n1.89\u00b10.12<\/td>\n<\/tr>\n
F(Fructose\/Glucose 30%)<\/td>\n4.63\u00b10.31<\/td>\n2.10\u00b10.16<\/td>\n<\/tr>\n
G(Fructose\/Glucose 40%)<\/td>\n4.47\u00b10.32<\/td>\n2.24\u00b10.12<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Values are expressed as mean \u00b1 SD for n=7 rats\/groups <\/em><\/p>\n

Group 1: Treated as control (100% feed) <\/em><\/p>\n

Group 2: Treated with 20% honey, 80% feed <\/em><\/p>\n

Group 3: Treated with 30% honey, 70% feed <\/em><\/p>\n

Group 4: Treated 40% honey, 60 feed <\/em><\/p>\n

Group 5: Treated with fructose\/glucose equivalent to amounts in 20% honey<\/em><\/p>\n

Group 6; Treated with fructose\/glucose equivalent to amounts in 30% honey. <\/em><\/p>\n

Group 7: Treated\u00a0 with fructose\/glucose equivalent to amounts in 40% honey. <\/em><\/p>\n

Fructose at higher amounts significantly (p<0.05) reduced hepatic HDL-cholesterol but increased (p<\/em><0.05) LDL-cholesterol.\u00a0 Honey increased (p<0.05) hepatic HDL-cholesterol at 40%, but LDL-cholesterol levels were minimally elevated (Table 2).<\/p>\n

Discussion<\/strong><\/p>\n

Honey is a biological product with very complex\u00a0 chemical composition (Busserolles, et al<\/em>., 2002). It is a popular viscous sweetener and a common household product used through out the world.\u00a0 From this research, high amounts of honey and fructose feeding\u00a0 caused significant increase in hepatic glucose level when compared with the control value.\u00a0 The present experiment confirms the hypertriglyceridaemic reaction induced by dietary fructose (Table 1).\u00a0 It is noteworthy that substituting honey for refined carbohydrates lowers the triacylglycerol levels.\u00a0 Honey reduced total cholesterol and increased high density lipoprotein cholesterol (HDL-C) in the liver tissue.\u00a0 This experiment is in agreement with previous studies (Yoghoobi, et al<\/em>., 2008; Al-Waili, 2004).\u00a0 Low density lipoprotein cholesterol levels were increased in the liver of experimental rats feed honey (p<\/em>>0.05) and fructose (p<\/em><0.05)\u00a0 compared with control (Table 2).<\/p>\n

Honey and fructose feeding alike increase the amounts of glucose, triacylglycerol and LDL-cholesterol but lower HDL-cholestgerol levels in the liver. \u00a0The results present a measure of fatty liver and associated fibrotic risk in both groups of experimental animals.\u00a0 The increased hepatic glucose level suggests a degree of (oxidative) stress.\u00a0 Further studies involving the metabolic activities of the liver during honey feeding are desirable in order to fully document the observed risks.<\/p>\n

Acknowledgements<\/strong><\/p>\n

The author is grateful to Odibo Ogbewi Kingsley, who was very useful during the study.\u00a0 Dr. I. Onyesom also contributed; thank you so much sir.<\/p>\n

References<\/strong><\/p>\n

    \n
  1. Al-Waili, N.S (2004). Natural honey lower plasma glucose, C- reactive protein, homocystein, and blood lipids in healthy, diabetic and hyperlipidemic subjects. Comparison with dextrose and sucrose.\u00a0 Med. Food<\/em> 7: 100 \u2013 107.<\/li>\n
  2. Bansal, V., Medhi, B. and Pandhi, P. (2005). Honey \u2013 A remedy rediscovered and its therapeutic utility. Kathmadu Uni. Med. J.<\/em> 3 (3) 11:305 \u2013 309.<\/li>\n
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  9. Molan P.C. (2001). Potential of honey in the treatment of wounds and burns. J. Clin. Dermatol<\/em>. 2:9-13.<\/li>\n
  10. Munstedt, K., Hoffmann, S., Hanenschild, A., Butte, M., Georgi, R.V. and Hackethal, A. (2009). Effect of honey on serum cholesterol and lipid values.\u00a0 Med. Food<\/em>. 12 (3): 624 \u2013 628.<\/li>\n
  11. Perez, R.A. (2002). Analysis of volatiles from Spanish honey by solid-phase microextraction and gas chromatography mass spectrometry. Agric. Food Chem<\/em>. 50: 2633 \u2013 2637.<\/li>\n
  12. Trinder, P. (1969). Determination of blood glucose using 4-aminophenazone as oxygen acceptor. Clin. Pathol<\/em>. 22 (2): 246-248.<\/li>\n
  13. Wang, T.Y., Chen, R.M., and Teng, L.E. (1996). Accuracy of serum lipid measurements in Taiwan using fresh human serum in a survey. Biomed. Lab. Sci<\/em>. 8: 129-134.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

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