Trials over two years were conducted using 1389 sweetpotato (Ipomoea batatas L.) genotypes collected from all over the world to characterize the polyphenolic composition in sweetpotato leaves. Wide variation was observed in relation to their total and individual leaf polyphenolic constituents. In all genotypes studied, the total polyphenol contents of sweetpotato leaf ranged from 1.42 to 17.1 g/100 g dry weight. The six different polyphenolic compounds were identified and quantified by NMR, FABMS, and RPHPLC analysis procedures. This is the first report of polyphenolic compositions in sweetpotato leaves. The relative levels of polyphenolic acids in sweetpotato leaves were as follows: 3,5-di-O-caffeoylquinic acid > 4,5-di-O-caffeoylquinic acid > chlorogenic acid (3-O-caffeoylquinic acid) > 3,4-di-O-caffeoylquinic acid > 3,4,5-tri-O-caffeoylquinic acid > caffeic acid. The highest 3,4,5-tri-O-caffeoylquinic acid and 4,5-di-O-caffeoylquinic acid occurred at 221 and 1183.30 mg/100 g dry weight, respectively.

The main objective of the study was to develop an alternative non-genetic rat model for type 2 diabetes (T2D). Six-week-old male Sprague-Dawley rats (190.56 ± 23.60 g) were randomly divided into six groups, namely: Normal Control (NC), Diabetic Control (DBC), Fructose-10 (FR10), Fructose-20 (FR20), Fructose-30 (FR30) and Fructose-40 (FR40) and were fed a normal rat pellet diet ad libitum for 2 weeks. During this period, the two control groups received normal drinking water whilst the fructose groups received 10, 20, 30 and 40% fructose in drinking water ad libitum, respectively. After two weeks of dietary manipulation, all groups except the NC group received a single injection (i.p.) of streptozotocin (STZ) (40 mg/kg b.w.) dissolved in citrate buffer (pH 4.4). The NC group received only a vehicle buffer injection (i.p.). One week after the STZ injection, animals with non-fasting blood glucose levels > 300 mg/dl were considered as diabetic. Three weeks after the STZ injection, the animals in FR20, FR30 and FR40 groups were eliminated from the study due to the severity of diabetes and the FR10 group was selected for the remainder of the 11 weeks experimental period. The significantly (p < 0.05) higher fluid intake, blood glucose, serum lipids, liver glycogen, liver function enzymes and insulin resistance (HOMA-IR) and significantly (p < 0.05) lower body weight, oral glucose tolerance, number of pancreatic β-cells and pancreatic β-cell functions (HOMA-β) of FR10 group demonstrate that the 10% fructose-fed followed by 40 mg/kg of BWSTZ injected rat can be a new and alternative model for T2D.

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Due to the high prevalence of diabetes worldwide, extensive research is still being performed to develop new antidiabetic agents and determine their mechanisms of action. Consequently, a number of diabetic animal models have been developed and improved over the years, of which rodent models are the most thoroughly described. These rodent models can be classified into two broad categories: 1) genetically induced spontaneous diabetes models; and 2) experimentally induced nonspontaneous diabetes models. The popularity of using experimentally induced nonspontaneous models for diabetes research over that of the genetically induced spontaneous models is due to their comparatively lower cost, ease of diabetes induction, ease of maintenance and wider availability. The various experimentally induced type 2 diabetes (T2D) rodent models developed over the last 30-plus years for both routine pharmacological screening and mechanistic diabetes-linked research trials include: adult streptozotocin (STZ)/alloxan rat models, neonatal STZ/alloxan models, partial pancreatectomy models, long-term high-fat (HF) diet-fed models, HF diet-fed STZ models, nicotinamide/STZ models, intrauterine growth retardation (IUGR) models, the STZ-induced progressive diabetic model and monosodium glutamate (MSG)-induced model. The use of these models, however, is not without limitations. A T2D model should ideally portray an identical biochemical blood profile and pathogenesis to T2D in humans. Hence, this review will comparatively evaluate experimentally induced rodent T2D models considering the above-mentioned criteria, in order to guide diabetes research groups to more accurately select the most appropriate models given their specific research requirements.