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Ayu. 2011 Jul-Sep; 32(3): 432–433.
PMCID: PMC3326898

Authors’ reply


We are pleased to know about the interest taken by the readers[1] in our research. To minimize the biasness in subjective parameters, all the chief complaints and associated complaints were graded on the basis of severity of the symptoms and the assessment was done on the basis of those grading; however, to avoid the lengthiness of the article, the accepted grading has not been shown in the present article. All the laboratory investigations are done in the Biochemical Laboratory associated with Institute for Post Graduate Teaching and Research in Ayurveda, Gujarat Ayurved University, Jamnagar wherein IQAS (Internal Quality Assurance) is carried out on a regular basis, for which the controls are procured from Roche Diagnostics, Germany, required for various biochemical investigations.

Improvement in diabetes mellitus has not been assessed only on the basis of fasting blood sugar parameter but improvement in allthe chief and associated complaints; decrease in fasting and postprandial blood sugar and serum Insulin levels including decrease in serum cholesterol, serum triglyceride and increase in serum HDL have also been taken as criteria for assessment. Glycosylated hemoglobin would have been a better parameter to monitor the long-term control of diabetes mellitus but due to financial limit it was not possible, hence in the future study it can be assessed. The level of glycosylated hemoglobin is increased in the red blood cells of individuals with poorly controlled diabetes mellitus. Since the glucose stays attached to hemoglobin for the life of the red blood cell (normally about 120 days), the level of glycosylated hemoglobin reflects the average blood glucose level over the past 3 months. Levels above 9% show poor control and levels above 12% show very poor control. It is commonly recommended that glycosylated hemoglobin be measured every 3 to 6 months in diabetics. While discussing the effect of therapy, it is the inference drawn by the authors that the compound formulation – MMV might have worked through proven action of its ingredients, as the drugs like Amalaki,[2] Shunthi,[3] Pippali,[4] Kiratatikta,[5] Rasanjana (Daruharidra),[6] Dadima,[7] Bilva,[8] Devadaru[9] are proven hypoglycemic due to which it may control hyperglycemia and prevent glucotoxicity; Gugulu,[10] Haritaki,[11] Amalaki,[2] Shunthi[12] are proven antihyperlipidemic, so by reducing extra fat, they may decrease insulin resistance and increase insulin sensitivity and also prevent lipotoxicity; and Amalaki,[2] Shunthi,[3] Maricha,[13] Dadima[7] are proven antioxidants, which may reduce the degree of stress signaling pathway.

The objective of the present study was only to investigate antihyperglycemic, antihyperlipidaemic, and insulin-releasing effect of ‘Mehamudgaravati’ so for fulfilling this objective only FBS, PPBS, lipid profile, and serum insulin were checked. Of course, the authors did not investigate on antioxidant and immunity parameters as it was not at all an area of focus of the present study and authors have just tried to justify the result on the basis of proven action of ingredients after quoting authentic references. Further, it has been described under the heading of probable mode of action. The data on serum insulin suggests the complex activity of the drug both insulin secretagaug and peripheral utilization. But it just gives an indication towards multi-target oriented focusing of the drug. The present study provides scope for future researchers to investigate the mode of action of the drug and to explore the antidiabetic, antihyperglycemic, and hypoglycemic activities of Mehamudgaravati through different experimental models and antioxidant activity through pharmaceutical studies.


1. Wiwanitkit V. Mehamudgaravati and type 2 diabetes mellitus. AYU. 2011;32:432. [PMC free article] [PubMed]
2. Vol. 3. New Delhi: Central Council of Research in Ayurveda and Siddha; 2001. Anonymous, Database on Medicinal plants used in Ayurveda; p. 11.
3. Ibid, ref. (2) 5:315.
4. Ibid, ref. (2) 3:472.
5. Ibid, ref. (2) 7:226.
6. Ibid, ref. (2) 1:120.
7. Ibid, ref. (2) 2:177.
8. Ibid, ref. (2) 1:79.
9. Ibid, ref. (2) 7:72.
10. Ibid, ref. (2) 2:233.
11. Ibid, ref. (2) 3:282.
12. Ibid, ref. (2) 5:315.
13. Ibid, ref. (2) 5:187.

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