According to the International Diabetes Federation (IDF), 350 million people will have diabetes globally by 2030, according to estimates. Although there is little scientific data on the use of Kigelia africana for ethnomedicine, it is widely used. Therefore, the goal of this research was to assess the plant’s anti-diabetic and antioxidant potential. For the study, Kigelia Africana leaf extracts in ethanol, methanol, and n-hexane were used. A total of 60 adult male albino rats weighing between 90 and 160 g were given alloxan diabetes. Cold normal saline was used to dissolve the alloxan. The presence of diabetes was determined after 72 hours, at which point the rats were divided into twelve (12) groups of five (5) each. Group 1 acted as the group 4 received 2.5 mg/kg b.wt of glibenclamide, group 6 received ethanol, methanol, and n-hexane leaves extract, while group 5, group 7, and group 9 received ethanol, methanol, and n-hexane fruit extract, respectively, at 500 mg/kg b.wt of the extracts. Group 2 was the untreated diabetic group. Groups 10 and 12 received an equal distribution of the leaf and fruit extracts. Following a 21-day oral feeding period, some biochemical and oxidative parameters were statistically analyzed in the rats. Standard methods for phytochemical screening for various bioactive compounds revealed the presence of reducing sugars, flavonoids, alkaloids, saponins, soluble carbohydrates, tannin, steroids, and glycosides. Proteins (13.9%), carbohydrates (63.5%), fats and oils (11.4%), and crude fiber were all present, according to proximate analysis. (2.2%). LD50 results indicated the extracts were secure.



Diabetes mellitus is a metabolic condition caused by a problem with insulin secretion, action, or both. Chronic hyperglycemia brought on by insulin insufficiency also causes disturbances in the metabolism of proteins, fats, and carbohydrates (Kumar et al., 2011).

When insulin-stimulated glucose uptake by fat and muscle fails to occur during diabetes, the blood glucose concentration stays high, which causes an increase in glucose uptake by insulin-independent tissue. Through a variety of interconnected non-enzymatic, enzymatic, and mitochondrial pathways, increased glucose flux both increases oxidant production and weakens antioxidant defenses (Klotz 2002; Mehta et al., 2006). These include increased hexosamine pathway activity (Kaneto et al., 2001), increased glucose autoxidation (Brownlee, 2001), increased methylglyoxal and advanced glycation end-product (AGEs) formation (Thornalley, 1998), and activation of protein kinase C isoforms (Inoguchi et al., 2000). increased flux along the polyol pathway ( Lee and Chung, 1999). The overproduction of superoxide by the mitochondrial electron transport system is the cause of these seemingly distinct mechanisms (Tushuizen et al., 2005). This oxidative stress caused by hyperglycemia leads to DNA damage, intracellular protein modification that alters gene expression, activation of the cellular transcription (NFK B), decreased nitric oxide production, and increased expression of cytokines, growth factors, and pro-coagulant and pro-inflammatory molecules (Palmer et al., 1988; Evans et al., 2002; Klotz, 2002; Taniyama and Griendling, 2003). According to Halliwell (1994), oxidative stress causes molecular and cellular tissue damage in a variety of human diseases, including diabetes mellitus. Diabetes results in lipid abnormalities. profiles, particularly a higher propensity for lipid peroxidation (Lyons, 1991), which is linked to an increased risk of atherosclerosis (Guigliano et al., 1996), a serious complication of diabetes mellitus. These patients have been found to have an enhanced oxidative stress, which is demonstrated by increased free radical production, lipid peroxidation, and decreased antioxidant status (Baynes, 1991).


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