This study analyzed the content of eight triterpenes (oleanolic acid, ursolic acid, arjunolic acid, asiatic acid, boswellic acid, corosolic acid, madecassic acid, and maslinic acid) in ten vegetables and eight fruits. These compounds at 0.5% were supplied to mice for 4 or 8 weeks. The bioavailability, tissue distribution, and antioxidative protection of these triterpenes were examined. Results showed that triterpenes were detected in eight vegetables and six fruits. Basil and brown mustard contained seven test triterpenes, in the range of 14-102 mg/100 g dry weight. The level of each triterpene in plasma, brain, heart, liver, kidney, colon, and bladder increased as the feeding period was increased from 4 weeks to 8 weeks (P < 0.05). Renal homogenates from mice with triterpene intake had greater antioxidative effects against glucose-induced glutathione loss and malondialdehyde and oxidized glutathione production when compared with those from control groups (P < 0.05). These data support that these triterpenes were absorbed and deposited in their intact forms, which in turn exerted in vivo antioxidative protection.

White. Central leptin increases insulin sensitivity in streptozotocin-induced diabetic rats. Am J Physiol Endocrinol Metab 282: E1084-E1091, 2002; 10.1152/ajpendo.00489.2001.-This study examined the effect of intracerebroventricular leptin on insulin sensitivity in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were cannulated in the lateral ventricle and, after recovery, administered either intravenous STZ (50 mg/kg) to induce diabetes or citrate buffer. Chronic leptin (10 g/10 l icv) or vehicle injections were administered daily for 14 days beginning 2 days after establishment of hyperglycemia in the diabetic animals. At the end of the 2 wk of injections, insulin sensitivity was measured by the steady-state plasma glucose (SSPG) method. Blood glucose concentrations were dramatically reduced and normalized by the 4th day in diabetic animals receiving intracerebroventricular leptin treatment. Diabetic animals exhibited insulin resistance, whereas intracerebroventricular leptin significantly enhanced insulin sensitivity, as indicated by decreased SSPG. Circulating leptin levels were not increased in animals injected with intracerebroventricular leptin. Thus the increased peripheral insulin sensitivity appears to be due solely to the presence of leptin in the brain, not to leptin acting peripherally. These data imply that inadequate central leptin signaling may lead to insulin resistance. intracerebroventricular leptin; insulin resistance; hyperglycemia THE INTERACTION BETWEEN LEPTIN AND INSULIN has been the subject of several investigations. Leptin is thought to be a signal that informs the brain about the size of the fat mass in the body. It acts as a satiety factor, decreasing food intake and increasing energy expenditure, or at least preventing the decrease in energy expenditure normally associated with a decrease in food intake (38). These effects lead to a decrease in body fat. In addition to these actions, leptin treatment enhances insulin sensitivity in normal rats, as indicated by increased insulin-stimulated glucose utilization in peripheral tissues (7,33,42). It also decreases plasma glucose and/or insulin concentrations of normal animals in the postabsorptive state. Leptin has been shown to directly inhibit insulin secretion (11), whereas insulin increases leptin release from adipocytes (25). Evidence indicates that glucose metabolism, rather than insulin itself, is the main determinant for leptin expression in adipose tissue (22). Moreover, in vivo and in vitro evidence suggests that leptin and insulin-signaling networks may be connected at several levels, such as insulin receptor substrates, or IRS; phosphatidylinositol 3-kinase, or PI 3-kinase; and mitogen-activated protein kinase, or MAPK (19,20,41). Therefore, leptin and insulin-signaling pathways may interact with each other.The effects of leptin on insulin sensitivity have been examined independently of peripheral insulin concentrations. Diabetic animals induced by streptozotocin (STZ), which selectively destroys insulin-producing...

Content of protocatechuic acid (PA) in eight locally available fresh fruits was analyzed, and the protective effects of this compound in diabetic mice were examined. PA at 1%, 2%, and 4% was supplied to diabetic mice for 8 weeks. PA treatments significantly lowered plasma glucose and increased insulin levels. PA treatments at 2% and 4% significantly lowered plasminogen activator inhibitor-1 activity and fibrinogen level; increased plasma activity of antithrombin-III and protein C; decreased triglyceride content in plasma, heart, and liver; elevated glutathione level and the retention of glutathione peroxidase and catalase activities in heart and kidney. PA treatments at 2% and 4% also significantly lowered plasma C-reactive protein and von Willebrand factor levels and reduced interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 levels in heart and kidney. These results support that protocatechuic acid could attenuate diabetic complications via its triglyceride-lowering, anticoagulatory, antioxidative, and antiinflammatory effects.

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Protocatechuic acid (PCA) at 2 or 4% was supplied to diabetic mice for 12 weeks. PCA treatments increased its deposit in organs and significantly reduced the plasma HbA1c level, the urinary glycative albumin level, and renal production of carboxymethyllysine (CML), pentosidine, sorbitol, and fructose (p < 0.05). However, PCA treatments only at 4% significantly decreased brain content of CML, pentosidine, fructose, and sorbitol (p < 0.05). PCA treatments at 2 and 4% significantly lowered renal activity and mRNA expression of aldose reductase and sorbitol dehydrogenase (p < 0.05), and PCA treatments only at 4% significantly enhanced renal glyoxalase I mRNA expression (p < 0.05). PCA treatments also dose-dependently decreased the renal level of type-IV collagen, fibronectin, and transforming growth factor-β1 (p < 0.05), as well as dose-dependently diminished renal protein kinase C (PKC) activity (p < 0.05); however, PCA treatments only at 4% suppressed renal mRNA expression of PKC-α and PKC-beta (p < 0.05). PCA treatments at 4% significantly restored renal mRNA expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ, as well as suppressed expression of the advanced glycation end-product receptor (p < 0.05). These findings suggest that the supplement of PCA might be helpful for the prevention or alleviation of glycation-associated diabetic complications.