The Repository @ St. Cloud State

Open Access Knowledge and Scholarship

Date of Award


Culminating Project Type

Starred Paper

Degree Name

Special Studies: M.A.




College of Science and Engineering

First Advisor

Marina Cetkovic-Cvrlje

Second Advisor

Heiko Schoenfuss

Third Advisor

Cassidy Dobson

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Keywords and Subject Headings

Type one diabetes, Garcinia kola, glycemia


Type 1 Diabetes (T1D) is an insulin-dependent autoimmune disease characterized by the T-cell mediated autoimmune destruction of insulin-producing pancreatic β-cells. This destruction results in hyperglycemia (elevated blood glucose levels), which causes metabolic imbalances, pathological changes in tissue, vascular complications and multi-organ damage. Pharmaceuticals used to treat T1D are expensive and not readily available in underdeveloped countries. It is therefore an imperative to study natural compounds with a potential hypoglycemic and anti-inflammatory properties, such as Garcinia kola seeds. The effect of aqueous Garcinia kola seed extract (GKE) on incidence and severity of T1D was studied in a multiple-low-dose streptozotocin (MLDSTZ)-induced mouse model of T1D. It is hypothesized that GKE treatment would decrease glycemia levels and reduce incidence of autoimmune mouse T1D. GKE was prepared by aqueous extraction, and C56Bl/6J male mice were exposed to 100 mg/kg/day of GKE via drinking water for a period of five weeks (from 7- to 12-weeks of age). At 8-weeks of age T1D was chemically induced with five consecutive injections of 40 mg/kg streptozotocin (STZ). Body weights and blood glucose levels were measured before STZ administration and bi-weekly from day 8 until day 29 post first STZ injection. The results showed that GKE treatment did not reduce body weights and glycemia levels; even a trend of elevated body weights and hyperglycemia levels was observed in GKE-treated mice. In addition, GKE exposure significantly increased T1D incidence in MLDSTZ-treated mice. In conclusion, this study, as the first examination of the anti-diabetogenic potential of aqueous GKE, did not confirm its potential in reducing hyperglycemia and preventing T1D.


I would like to thank Dr. Cetkovic for taking me on as a graduate student, Shana Rogan, my co-graduate student working on this project and all of the undergraduate students who worked to help make this research project possible.



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