Skip to main content


We're creating a new version of this page. See preview

  • Letter to the Editor
  • Open Access

Zinc and curcumin lower arylsulfatses and some metabolic parameters in streptozotocin-induced diabetes

Journal of Diabetes & Metabolic Disorders201716:11

  • Received: 12 October 2016
  • Accepted: 6 March 2017
  • Published:


In rats with induced diabetes, Zinc and curcumin treatment showed a significant increase of catalase and a significant decrease of glucose, lipid profile components and arylsulphatases activity compared to the untreated rats. We suggest that dietary zinc and curcumin are promising protective agents for reducing the metabolic defect of diabetes.


  • Curcumin
  • Diabetic Group
  • Experimental Diabetes
  • Arylsulfatase
  • Curcumin Treatment

Dear Editor;

Diabetes mellitus is a metabolic disease and the pathogenesis of diabetes mellitus is implicated in the oxidative stress and the generation of superoxide free radicals [1]. Various small molecules have been investigated for their ability to ameliorate the diabetes. One such molecule is curcumin (Cur) that has various health beneficial properties such as anti-inflammatory, anticarcinogenic, antiviral, hypolipidemic and antiinfectious activities [2, 3]. The 2nd molecule is the zinc (Zn) salt as an essential trace element. The disturbances of its homeostasis seem to be associated not only with diabetes, but also with others [4]. Recently, it was reported that the lysosomal enzymes arylsulfatases were significantly changed in experimental diabetes [5]. In fact, the treatment of diabetes through food sources is valuable around the world. Therefore, the present study is undertaken to throw the light on the effect of Zn and Cur on rats with experimental diabetes rats through studying the effect on some lipid components and arylsulfatases as important parameters, which are implicated in different biological functions.

Male albino rats (120–160 g Bwt) were kept on a balanced ration with water ad libitum for acclimatization. Experimental diabetes was induced in overnight fasted rats by intraperitoneal injection of a single dose of streptozotocin (STZ) as 60 mg/kg Bwt. Rats with a serum glucose level 218 mg/dl were considered as rats with diabetes. The daily intake of Zn sulfate (100 mg/kg Bwt) and was administrated orally in non-ionized water for 60 days. Cur was suspended in saline and administrated orally by a gavage 80 mg/kg Bwt Cur suspended daily in saline for 60 days. The rats were grouped randomly into eight equal groups as the non-diabetic (control group), the diabetic group, Zn non-diabetic group, Zn diabetic group, Cur non-diabetic group, Cur diabetic group. The last two groups that belong to Zn and Cur non-diabetic and diabetic group received 50 and 40 mg/kg Bwt, respectively as a daily for 60 days. The animals were deprived of food overnight and sacrificed by decapitation. Blood was collected from the eye canthus in tubes containing potassium oxalate and sodium fluoride mixture for estimation of plasma glucose (PG). Liver or pancreas tissues were weighed, homogenized in10 mM Tris HCl buffer, pH 7.0 and centrifuged at 4000 rpm for 15 min at 4 °C. The clear supernatant was obtained to measure the activities of catalase [6], total protein [7] and both arylsulfatase A (ASA) and arylsulfatase B (ASB) [8]. ASA and ASB were fractionated by DEAE-cellulose chromatography as described previously [8]. Insulin was assayed in the homogenate of pancreas of all groups according to instruction of Sigma-Aldrich insulin ELISA kit. Serum total cholesterol (STC) was determined by cholesterol oxidase and peroxidase [9]. Serum triacylglycerol (STG) was determined as described previously [10]. Serum LDL cholesterol (SLDL-c) and HDL cholesterol (SHDL-c) levels were estimated as that described previously [11]. The obtained data during the experimental period were statistically analyzed by the paired sample T-test (SPSS version 16).

A significant increase of plasma glucose was noted after one and 60 days of STZ injection. Oral administration of Zn, Cur and a combination of both showed a significant effect on blood glucose levels (1.9 fold-increase). Similar results were obtained by the effect of Cur, whereas an increase of plasma sugar level of 4.7 folds in day one was changed to be only 1.7 fold after 60 days of STZ-treatment. Interestingly, on treating the rats by both Zn and Cur, the noticed significant change of plasma sugar level in day one was changed to be non-significant at 60 days of STZ-treatment (Table 1). A reversed tendency to that of plasma glucose was shown on measuring the insulin content of pancreatic homogenate of animals from the different groups. The rats with diabetes showed a significant decrease (4.4 fold) in insulin compared to control (p < 0.001). Insulin level showed a non-significant change after treatment with Zn and Cur. In addition, a significant increase in the levels of serum total cholesterol (STC) and triacylglycerol (STG) in the diabetic groups was noticed in comparison to the non-diabetic groups. Comparison of the diabetic groups versus the non-diabetic groups showed a significant decrease in both SHDL-c and SLDL-c levels in the diabetic groups and a significant increase after treatment with Zn and Cur (Table 1). For studying the effect of Zn and Cur on free radical production, the activity of catalase was measured in both plasma and liver. It presented a significant decrease in diabetic compared to control rats. The effect of Zn and Cur showed a significant increase of the specific activity in serum and hepatic catalase compared to STZ-induced diabetic rats (p < 0.05). Furthermore, there is a significant increase in the specific activities of ASA and ASB in both serum and liver in the rats of the diabetic group compared to control (Table 2). Zn and Cur administration decrease it significantly compared to the diabetic group (p < 0.05). The significant increase of catalase by Zn may be attributed to the competition of Zn to both iron and copper for binding to cell membranes and thus decreasing the production of OH- group [12]. This group in turn stimulates the peroxidation of membrane lipids and hence the outflow of lysosomal constituents into cytosol [13]. The role of combination of both Zn and Cur in diabetes showed a highly significant effective result than the use of Zn or Cur alone. Taken together, we suggest that Zn and Cur have an effective and a protective role against the effect of diabetes—produced radicals on lysosomes. Dietary Zn and Cur are promising protective agents with a potential therapeutic approach to diabetes.
Table 1

Effect of Zn and curcumin on Lipid Profile distribution


Plasma glucose (PG, mg/dl)

Serum total cholesterol

Serum triacylglycerol

Serum LDL

Serum HDL


111.84 ± 2.56

50.25 ± 1.54

37.2 ± 1.73

63.75 ± 3.20

106.56 ± 3.04


381.81 ± 15.12**

137.02 ± 7.04**

635.63 ± 29.57**

50.71 ± 6.22**

41.79 ± 1.38**

Zn non-diabetic

73.61 ± 2.21*

32.67 ± 1.31*

37.9 ± 1.01

72.16 ± 3.40

79.24 ± 2.83*

Zn-treated diabetic

138.59 ± 7.81*

60.34 ± 3.67*

116.40 ± 3.54*

61.98 ± 4.44

99.04 ± 3.19

Cur non-diabetic

74.47 ± 2.99*

47.49 ± 1.45

23.95 ± 0.86*

56.70 ± 2.24

99.99 ± 2.19

Cur-treated diabetic

124.88 ± 4.36*

59.13 ± 3.07*

30.95 ± 1.39*

28.51 ± 3.60*

82.61 ± 3.40*

Zn and Cur non-diabetic

111.08 ± 4.39

47.15 ± 1.60

34.53 ± 1.66

58.09 ± 3.01

98.33 ± 2.40

Zn and Cur- treated diabetic

118.22 ± 4.90

51.47 ± 1.37

41.3 ± 2.30

38.88 ± 2.56*

82.89 ± 2.50*

The mean values of the serum level (mg/dl) of total cholesterol, triacylglycerol and the lipoproteins LDL and HDL in control, diabetic, Zn- and curcumin-treated diabetic groups. The values are the means of 12 rats ± SE. Significance: *p < 0.05 and **p < 0.001 compared to control

Table 2

Effect of Zn and Cur on the specific activity of catalase (units/mg protein) and arylsulfatases ASA and ASB (nmol product/h/mg protein)


Serum Catalase​(x 104)

Hepatic Catalase​(x104)

Serum ASA

Hepatic ASA

Serum ASB

Hepatic ASB


1.09 ± 0.05

28.5 ± 1.4

12.01 ± 0.74

226.78 ± 10.25

23.28 ± 1.50

505.82 ± 23.03


0.49 ± 0.03**

4.4 ± 0.4**

25.58 ± 0.89**

555.36 ± 52.49**

34.24 ± 1.90*

627.79 ± 53.18**

Zn non-diabetic

1.00 ± 0.03

36.4 ± 2.8*

15.25 ± 0.81

268.04 ± 6.78*

34.69 ± 1.62*

531.61 ± 17.67*

Zn-treated diabetic

0.97 ± 0.03

34.1 ± 1.5*

9.53 ± 0.78*

214.66 ± 3.99*

21.42 ± 1.02

408.94 ± 15.37*

Cur non-diabetic

0.88 ± 0.03

36.9 ± 2.0*

14.86 ± 0.51

261.32 ± 8.47*

33.26 ± 2.08*

604.90 ± 11.17*

Cur-treated diabetic

1.03 ± 0.03

47.1 ± 1.9*

11.13 ± 0.66

260.33 ± 10.70*

32.87 ± 1.96*

431.83 ± 22.81*

Zn and Cur non-diabetic

1.01 ± 0.03

35.8 ± 1.5*

12.46 ± 0.23

174.60 ± 10.17*

31.10 ± 1.11*

501.37 ± 17.75

Zn and Cur-treated diabetic

1.00 ± 0.02

36.2 ± 2.5*

9.32 ± 0.40*

150.59 ± 11.39*

20.28 ± 1.14

333.67 ± 22.74*

The values are the means of 12 rats ± SE. Significance: *p < 0.05 and **p < 0.001 compared to control



Arylsulfatase A


Arylsulfatase B


Body weight




Plasma glucose


Serum high density lipoprotein cholesterol


Serum low density lipoprotein cholesterol


Serum total cholesterol


Serum total triacylglycerol





The authors thank the technical staff of Department of Biochemistry, Faculty of Science, Alexandria University, Egypt for their helpful assistance.


This letter was extracted from an ongoing research project that is conducted by Mahmoud Balbaa and coworkers. This project was partially supported by Alexandria University, Egypt.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Authors’ contributions

MB participated in acquisition of the data, study concept and design, data interpretation, data analysis and critical revision of the manuscript for important intellectual content. ME participated in acquisition of the data, study concept and design, analysis and interpretation of the data, drafting of the manuscript and critical revision of the manuscript for important intellectual content. NT participated in the interpretation of the data and drafting of the manuscript. AM participated in the interpretation of the data. All authors read and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

This article is original and was not published in any other journal. We have declared to give a right to publish in Journal of Diabetes & Metabolic Disorders.

Ethics approval and consent to participate

All the experimental procedures were conducted according to the animal protocols approved by the Ethics Committee of Faculty of Science, Alexandria University, Egypt.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

Departments of Biochemistry, Faculty of Science, Alexandria University, Moharram Bey, 21511 Alexandria, Egypt
Edfina Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt


  1. Firoozrai M, Nourbakhsh M, Razzaghy-Azar M. Erythrocyte susceptibility to oxidative stress and antioxidant status in patients with type 1 diabetes. Diabetes Res Clin Pract. 2007;77:427–32.View ArticlePubMedGoogle Scholar
  2. Joe B, Vijaykumar M, Lokesh BR. Biolgical properties of curcumin-cellular and molecular mechanisms of action. Crit Rev Food Sci Nutr. 2009;44:97–111.View ArticleGoogle Scholar
  3. Best L, Elliott AC, Brown PD. Curcumin induces electrical activity in rat pancreatic beta-cells by activating the volume-regulated anion channel. Biochem Pharmacol. 2007;73:1768–75.View ArticlePubMedGoogle Scholar
  4. Jansen J, Karges W, Rink L. Zinc and diabetes- clinical links and molecular mechanisms. J Nutr Biochem. 2009;20:399–417.View ArticlePubMedGoogle Scholar
  5. Samarji R, Balbaa M. Anti-diabetic activity of different oils through their effect on arylsulfatases. J Diabetes Metab Disord. 2014;13:116. doi:10.1186/s40200-014-0116-z.View ArticlePubMedPubMed CentralGoogle Scholar
  6. Aebi H. Catalase in vitro. Methods Enzymol. 1984;105:121–26.View ArticlePubMedGoogle Scholar
  7. Doumas BT, Bayse DD, Carter R, Peters Jr T, Schaffer R. A candidate reference method for determination of total protein in serum. I. Development and validation. Clin Chem. 1981;27:1642–50.PubMedGoogle Scholar
  8. Balbaa M, El-Kersh M, Mansour H, Yacout G, Ismail M, Malky A, Bassiouny K, Abdel-Monem N, Kandeel K. Activity of some hepatic enzymes in schistosomiasis and concomitant alteration of arylsulfatase B. J Biochem Mol Biol. 2004;37:223–28.PubMedGoogle Scholar
  9. Flegg HM. Cholesterol reagent. Ann Clin Biochem. 1973;10:79–84.View ArticleGoogle Scholar
  10. Bucolo G, David H. Quantitative determination of serum triglycerides by the use of enzymes. Clin Chem. 1973;19:476–82.PubMedGoogle Scholar
  11. Burestein M, Scholnick HR, Morfin R. Rapid method for the isolation of lipoproteins from human serum by precipitation with polyanions. J Lipid Res. 1970;11:583–93.Google Scholar
  12. Prasad AS. Clinical, immunological, anti-inflammatory and anti-oxidant roles of zinc. Exp Gerontol. 2008;43:370–77.View ArticlePubMedGoogle Scholar
  13. Boya P, Kroemer G. Lysosomal membrane permeabilization in cell death. Oncogene. 2008;27:6434–51.View ArticlePubMedGoogle Scholar


© The Author(s). 2017