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We evaluated antihyperglycemic and anti-obese effects of Panax ginseng berry extract and its major constituent, ginsenoside Re, in obese diabetic C57BL/6J ob/ ob mice and their lean littermates. Animals received daily intraperitoneal injections of Panax ginseng berry extract for 12 days. On day 12, 150 mg/kg extract-treated ob/ob mice became normoglycemic (137 +/- 6.7 mg/dl) and had significantly improved glucose tolerance. The overall glucose excursion during the 2-h intraperitoneal glucose tolerance test decreased by 46% (P < 0.01) compared with vehicle-treated ob/ob mice. The improvement in blood glucose levels in the extract-treated ob/ ob mice was associated with a significant reduction in serum insulin levels in fed and fasting mice. A hyperinsulinemic-euglycemic clamp study revealed a more than twofold increase in the rate of insulin-stimulated glucose disposal in treated ob/ ob mice (112 +/- 19.1 vs. 52 +/- 11.8 micromol x kg(-1) x min(-1) for the vehicle group, P < 0.01). In addition, the extract-treated ob/ob mice lost a significant amount of weight (from 51.7 +/- 1.9 g on day 0 to 45.7 +/- 1.2 on day 12, P < 0.01 vs. vehicle-treated ob/ob mice), associated with a significant reduction in food intake (P < 0.05) and a very significant increase in energy expenditure (P < 0.01) and body temperature (P < 0.01). Treatment with the extract also significantly reduced plasma cholesterol levels in ob/ob mice. Additional studies demonstrated that ginsenoside Re plays a significant role in antihyperglycemic action. This antidiabetic effect of ginsenoside Re was not associated with body weight changes, suggesting that other constituents in the extract have distinct pharmacological mechanisms on energy metabolism.

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The acquired immunodeficiency syndrome (AIDS) is a result of human immunodeficiency virus (HIV) infection which subsequently leads to significant suppression of immune functions. AIDS is a significant threat to the health of mankind, and the search for effective therapies to treat AIDS is of paramount importance. Several chemical anti-HIV agents have been developed. However, besides the high cost, there are adverse effects and limitations associated with using chemotherapy for the treatment of HIV infection. Thus, herbal medicines have frequently been used as an alternative medical therapy by HIV positive individuals and AIDS patients. The aim of this review is to summarize research findings for herbal medicines, which are endowed with the ability to inhibit HIV. In this article, we will emphasize a Chinese herbal medicine, Scutellaria baicalensis Georgi and its identified components (i.e., baicalein and baicalin), which have been shown to inhibit infectivity and replication of HIV. Potential development of anti-AIDS compounds using molecular modeling methods will also be discussed.

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Afferent sensory fibers are the primary neuroanatomic link between nutrient-related events in the gastrointestinal tract and the central neural substrates that modulate ingestion. In this study, we evaluated the peripheral gastric effects of leptin (OB protein) on brain stem neuronal activities using an in vitro neonatal rat preparation. We also tested gastric leptin effects as a function of age in neonates. For ∼33% of the nucleus tractus solitarius units observed, gastric leptin (10 nM) produced a significant activation of 188.2 ± 8.6% (mean ± SE) compared with the control level of 100% ( P < 0.01). Concentration-dependent leptin effects have also been shown. The remaining neurons (67%) had no significant response to gastric leptin application. Next, we evaluated the peripheral gastric effects of leptin (10 nM) on brain stem unitary activity in three different age groups (1–2 days old, 3–5 days old, and 7–8 days old) of neonatal rats. In the 1- to 2-day-old and the 3- to 5-day-old groups, we observed that response ratios and activity levels were similar. However, there was a significant difference between the 7- to 8-day-old group and the two younger age groups in both the response ratios and the activation levels. The percentage of activation responses increased from ∼26% in the 1- to 2-day-old and the 4- to 5-day-old age groups to 70% in the 7- to 8-day-old group ( P < 0.05). The level of activation increased from 168.3 ± 2.7% (compared with the control level) in the 1- to 2-day-old and the 4- to 5-day-old age groups to 231.4 ± 11.9% in the 7- to 8-day-old group ( P < 0.01). Our data demonstrate that peripheral gastric leptin modulates brain stem neuronal activity and suggest that gastric leptin has a significantly stronger effect in the 7- to 8-day-old animals than in the younger neonates.

Leptin (OB protein) elicits a neuroendocrine response to starvation and states of nutritional abundance to stabilize the proportion of body fat. Leptin has dramatic effects on food intake and energy expenditure in adult and juvenile rodents. However, whether the neonatal period is associated with the development of an effective leptin feedback system is still not known. In this study, we evaluated the effects of peripherally administered leptin on body weight changes in neonatal rats during the early suckling period (from birth to 10 d). Our results show that daily i.p. injections of leptin (0.3 g/g and 1.0 g/g) to neonatal rats led to a significant reduction in weight gain over 10 d compared with the control group (p Ͻ 0.01 and p Ͻ 0.01, respectively). Concomitant with a reduction in weight gain, retroperitoneal fat pad weight also significantly decreased in the leptin-treated group. Our data indicate that the potential for energy balance regulation by leptin occurs in the first day after birth. In addition, we also observed that 3 d after discontinuing leptin treatment, the body weight as well as the fat pad weight of leptin-treated pups returned to the control level. Our results demonstrate that leptin reduces body weight gain in neonatal rats. Leptin, the secreted product of the obese (ob) gene, regulates food intake and energy expenditure (1, 2). Leptin may increase energy expenditure by enhancing systemic (3) and brown adipose tissue glucose utilization (4). Thus far, adipose tissue (5) as well as the stomach (6) have been identified as sites of leptin synthesis. Leptin acts as a link in the feedback loop between adipose tissue and satiety centers in the hypothalamus, resulting in a decrease in appetite and an increase in energy expenditure (5, 6). However, it is also possible that sources of leptin other than adipose tissue play a similar role. For example, the epithelium of the gastric fundus and gastric glands not only synthesize and store leptin, but also secrete leptin in response to food intake (7). Arterially injected leptin increases gastric vagal nerve activity (8), and these afferent inputs link nutrient-related events in the gastrointestinal tract to the CNS areas that mediate the control of food intake (9, 10). We recently observed that leptin applied to the gastric mucosa increases neuronal activity in the nucleus tractus solitarius of the brain stem, the first relay station of autonomic afferent inputs (11).There is evidence that leptin regulates body weight during the postnatal period (12, 13). However, in young rodents, unlike in adults, leptin decreases body weight gain via increasing energy expenditure by varying the metabolic rate (13). In suckling pups (from birth to 21 d), because food intake is restricted by the maternal milk supply, the energy expended for thermoregulation limits the energy left for growth and fat deposition (14). Moreover, endogenous leptin levels of postnatal rats correspond to changes in dietary fat intake. Trottier et al. (15) reported that suckling rat pups fe...