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Ocimum sanctum leaf extracts stimulate insulin secretion from perfused pancreas, isolated islets and clonal pancreatic β-cells

J M A Hannan

J M A Hannan Diabetes Research Group, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland BT52 1SA, UK
Department of Pharmacology, Biomedical Research Group, BIRDEM, Dhaka-1000, Bangladesh

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L Marenah

L Marenah Diabetes Research Group, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland BT52 1SA, UK
Department of Pharmacology, Biomedical Research Group, BIRDEM, Dhaka-1000, Bangladesh

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L Ali

L Ali Diabetes Research Group, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland BT52 1SA, UK
Department of Pharmacology, Biomedical Research Group, BIRDEM, Dhaka-1000, Bangladesh

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B Rokeya

B Rokeya Diabetes Research Group, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland BT52 1SA, UK
Department of Pharmacology, Biomedical Research Group, BIRDEM, Dhaka-1000, Bangladesh

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P R Flatt

P R Flatt Diabetes Research Group, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland BT52 1SA, UK
Department of Pharmacology, Biomedical Research Group, BIRDEM, Dhaka-1000, Bangladesh

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Y H A Abdel-Wahab

Y H A Abdel-Wahab Diabetes Research Group, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland BT52 1SA, UK
Department of Pharmacology, Biomedical Research Group, BIRDEM, Dhaka-1000, Bangladesh

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Ocimum sanctum leaves have previously been reported to reduce blood glucose when administered to rats and humans with diabetes. In the present study, the effects of ethanol extract and five partition fractions of O. sanctum leaves were studied on insulin secretion together with an evaluation of their mechanisms of action. The ethanol extract and each of the aqueous, butanol and ethylacetate fractions stimulated insulin secretion from perfused rat pancreas, isolated rat islets and a clonal rat β-cell line in a concentration-dependent manner. The stimulatory effects of ethanol extract and each of these partition fractions were potentiated by glucose, isobutylmethylxanthine, tolbutamide and a depolarizing concentration of KCl. Inhibition of the secretory effect was observed with diazoxide, verapamil and Ca²⁺ removal. In contrast, the stimulatory effects of the chloroform and hexane partition fractions were associated with decreased cell viability and were unaltered by diazoxide and verapamil. The ethanol extract and the five fractions increased intracellular Ca²⁺ in clonal BRIN-BD11 cells, being partly attenuated by the addition of verapamil. These findings indicated that constituents of O. sanctum leaf extracts have stimulatory effects on physiological pathways of insulin secretion which may underlie its reported antidiabetic action.

Article Type:: Research Article

DOI:: https://doi.org/10.1677/joe.1.06615

Volume/Issue:: Volume 189: Issue 1

Free access

Androgen signaling pathways driving reproductive and metabolic phenotypes in a PCOS mouse model

Ali Aflatounian

Ali Aflatounian Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia

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Melissa C Edwards

Melissa C Edwards Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia
Andrology Laboratory, ANZAC Research Institute, University of Sydney, Concord Hospital, Sydney, New South Wales, Australia

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Valentina Rodriguez Paris

Valentina Rodriguez Paris Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia

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Michael J Bertoldo

Michael J Bertoldo Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia
Laboratory for Ageing Research, School of Medical Sciences, University of New South Wales Sydney, New South Wales, Australia

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Reena Desai

Reena Desai Andrology Laboratory, ANZAC Research Institute, University of Sydney, Concord Hospital, Sydney, New South Wales, Australia

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Robert B Gilchrist

Robert B Gilchrist Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia

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William L Ledger

William L Ledger Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia

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David J Handelsman

David J Handelsman Andrology Laboratory, ANZAC Research Institute, University of Sydney, Concord Hospital, Sydney, New South Wales, Australia

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Kirsty A Walters

Kirsty A Walters Fertility and Research Centre, School of Women’s & Children’s Health, University of New South Wales Sydney, New South Wales, Australia
Andrology Laboratory, ANZAC Research Institute, University of Sydney, Concord Hospital, Sydney, New South Wales, Australia

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As the mechanistic basis of polycystic ovary syndrome (PCOS) remains unknown, current management relies on symptomatic treatment. Hyperandrogenism is a major PCOS characteristic and evidence supports it playing a key role in PCOS pathogenesis. Classically, androgens can act directly through the androgen receptor (AR) or, indirectly, following aromatization, via the estrogen receptor (ER). We investigated the mechanism of androgenic actions driving PCOS by comparing the capacity of non-aromatizable dihydrotestosterone (DHT) and aromatizable testosterone to induce PCOS traits in WT and Ar-knockout (ARKO) mice. DHT and testosterone induced the reproductive PCOS-like features of acyclicity and anovulation in WT females. In ARKO mice, DHT did not cause reproductive dysfunction; however, testosterone treatment induced irregular cycles and ovulatory disruption. These findings indicate that direct AR actions and indirect, likely ER, actions of androgens are important mediators of PCOS reproductive traits. DHT, but not testosterone, induced an increase in body weight, body fat, serum cholesterol and adipocyte hypertrophy in WT mice, but neither androgen induced these metabolic features in ARKO mice. These data infer that direct AR-driven mechanisms are key in driving the development of PCOS metabolic traits. Overall, these findings demonstrate that differing PCOS traits can be mediated via different steroid signaling pathways and indicate that a phenotype-based treatment approach would ensure effective targeting of the underlying mechanisms.