Cladodes from Nopalea cochenillifera (L.) Salm-Dyck (Cactaceae) attenuate postprandial glycaemia without markedly influencing α-glucosidase activity.

Although the cladodes of Nopalea cochenillifera are used in Mexican traditional medicine to treat diabetes and various other diseases, its antihyperglycaemic properties, phenolic content, and antioxidant activity are not well documented. Thus, we determined the activity of a single dose of fresh, blended cladodes on postprandial glycaemia in rats after a starch load. We prepared a methanolic extract of N. cochenillifera cladodes and measured its phenolic content, antioxidant capacity, and α-glucosidase inhibitory activity. The antihyperglycaemic effect of blended cladodes was similar to that of acarbose when considering the changes in glucose levels from baseline. Furthermore, the methanolic extract contained a considerable amount of phenolic compounds and exhibited antioxidant activity in the DPPH assay, but did not markedly inhibit α-glucosidase and had a low antioxidant effect in the ABTS test.

Lupin protein isolate improves insulin sensitivity and steatohepatitis in vivo and modulates the expression of the Fasn, Gys2, and Gsk3b genes.

Although studies on lupin protein isolate (LPI) have indicated the presence of a preventive effect on insulin resistance (IR) and lipid disturbances, their influence on established pathological traits has received little attention. Here, we evaluated the in vivo effects of LPI on IR and steatohepatitis as well as its influence on genes involved in lipid and carbohydrate metabolism. We first induced IR and steatohepatitis in rats by maintaining them on a high-fat diet for 5 weeks. Thereafter, we administered LPI to the rats daily for 3 weeks. LPI improved insulin sensitivity (AUC: 6,777 ± 232 vs. 4,971 ± 379, p < .05, pre- vs. post-treatment values) and reduced glucose and triglyceride levels by one-third. In addition, LPI-treated rats exhibited attenuated steatohepatitis. At the molecular level, LPI treatment reduced liver Fasn gene expression substantially but increased Gys2 and Gsk3b levels. We concluded that the hypolipidemic and hypoglycemic activities of LPI may be caused by reduced liver lipogenesis and modulation of insulin sensitization mechanisms.

Analysis of hepatic transcriptome modulation exerted by γ-conglutin from lupins in a streptozotocin-induced diabetes model.

Lupinus albus γ-conglutin is proposed to positively affect glucose metabolism through inhibition of hepatic glucose production and insulin-mimetic activity; however, the action mechanism is not entirely known. Besides, most studies had focused on its effect on molecular targets directly related to glucose metabolism, and few studies have investigated how γ-conglutin may affect the liver gene expression or if it plays a role in other metabolic processes. Therefore, we investigated the influence of γ-conglutin on the liver transcriptome of streptozotocin-induced diabetic rats using DNA microarrays, ontological analyses, and quantitative PCR. Of the 22,000 genes evaluated, 803 and 173 were downregulated and upregulated, respectively. The ontological analyses of the differentially expressed genes revealed that among others, the mitochondria, microtubules, cytoskeleton, and oxidoreductase activity terms were enriched, implying a possible role of γ-conglutin on autophagy. To corroborate the microarray results, we selected and quantified, by PCR, the expression of two genes associated with autophagy (Atg7 and Snx18) and found their expression augmented two and threefold, respectively; indicating a higher autophagy activity in animals treated with γ-conglutin. Although complementary studies are required, our findings indicate for the first time that the hypoglycaemic effects of γ-conglutin may involve an autophagy induction mechanism, a pivotal process for the preservation of cell physiology and glucose homeostasis.