Explore chapters and articles related to this topic
Inhibiting the Absorption of Dietary Carbohydrates and Fats with Natural Products
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Delaying intestinal glucose absorption is an important therapeutic strategy to fight metabolic syndrome because it decreases postprandial glycemia, decreases insulin resistance, evokes mild loss of body weight, and improves serum lipid profiles.55 Aqueous extract from fruits of Siraitia grosvenorii (Swingle) C. Jeffrey ex A.M. Lu & Z.Y. Zhang given intragastrically and prophylactically to Wistar rats at a single dose of 0.1 g/kg decreased postprandial glycaemia when administered with oral load of maltose.56 From this extract, a mixture of triterpene glycosides at a dose of 0.1 g/kg decreased maltose-induced, postprandial glycaemia to 70% after 30 minutes.56 This fraction inhibited in vitro the enzymatic activity of rat intestinal maltase with an IC50 value equal to 5 mg/mL.56 From this fraction, the triterpene saponins mogroside V. (Figure 1.11) inhibited rat-intestinal maltase in vitro with an IC50 of 18 mg/mL.56 It should be noted that peak blood glucose values in rats are obtained much earlier (15–45 minutes) than in human subjects (around 60 minutes).57 Being nontoxic, the fruits of Siraitia grosvenorii (Swingle) C. Jeffrey ex A.M. Lu & Z.Y. Zhang could, be incorporated in the diet of subjects with metabolic syndrome. Clinical studies in this direction are needed.
Epstein–Barr Virus and Treatment of Its Infection
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Tarun Jha, Amit Kumar Halder, Nilanjan Adhikari
Forty-eight natural and semisynthetic cycloartane-type and related triterpenoids were evaluated for their inhibitory effects on EBV-EA activation induced by the tumor promoter TPA in Raji cells (Kikuchi et al. 2007). SAR analysis revealed that six compounds (containing a C-24 hydroxylated side chain) showed considerable inhibitory effects (IC50 values of 6.1–7.4 μM). The SAR also showed that the 3-oxo group exerts almost no, or less, influence on the activity than the 3β-hydroxy group. Feruloylation decreases the activity. Compound 72 (Figure 6.9) was, however, found to be the most potent compound. Seventeen lanostane-type triterpene acids were isolated from the epidermis of the sclerotia of Poria cocos belonging to the Polyporaceae family (Akihisa et al. 2007e), which showed an inhibitory effect on the EBV-EA activation induced by TPA in Raji cells. Most of these compounds showed inhibitory effects, with IC50 values ranging from 195 to 340 mol ratio/32 pmol TPA; poricoic acid (73, Figure 6.9) had the highest activity. Thirteen anthraquinones and saccharide fatty acid esters isolated from a methanol extract of the fruits of Morinda citrifolia belonging to the Rubiaceae family were examined by Akihisa et al. (2007c) and found to have moderate inhibitory effects (IC50 values ranging from 386 to 578 mol ratio/32 pmol TPA). The most potent compound among these was 1, 5, 15-tri-O-methyl morindol (74, Figure 6.9). These authors (Akihisa et al. 2007b) also evaluated some cucurbitane glycosides against the TPA-induced EBV-EA activation and reported inhibitory effects with IC50 values ranging from 346 to 400 mol ratio/32 pmol TPA. Mogroside IIIA2 (75, Figure 6.9) was found to be the most potent among all.
Nutrition in the management of type 2 diabetes mellitus: review
Published in Archives of Physiology and Biochemistry, 2021
The main compound isolated from Siraitia grosvenori Swingle (Luo han kuo) fruit, native to China. It has been used as a natural sweetening agent for centuries and has been reported to be beneficial for the diabetic population (Zhou et al.2009). The hypoglycaemic and hypolipidemic effects of mogroside-rich extract (MGE) and its possible mechanisms were investigated in a model of T2DM, induced by an HFD in combination with STZ. Intragastrically administration of MGE at two doses 150 and 300 mg/kg for 5 weeks to diabetic mice showed a prominent reduction of the fasting blood glucose (FBG), glycated serum protein (GSP), serum insulin, homeostasis model assessment-insulin resistance (HOMA-IR), and serum atherogenic lipid profiles in a dose-dependent manner. On the other hand, MGE at high dose (300 mg/kg) exhibited significant increases in the anti-atherogenic lipid profile, insulin sensitivity, glucose, and insulin tolerance capacity. Moreover, hepatocyte polymorphism, lipid accumulation, and steatosis were ameliorated and restored to near normal at the high dose. Also, hepatic 5'AMP-activated protein kinase (AMPK) signalling was dose-dependently activated. Accordingly, the mRNA levels of hepatic gluconeogenic and lipogenic genes were down-regulated and fat oxidation-associated genes were up-regulated. These results suggest that the hypoglycaemic and hypolipidaemic activities of MGE are probably due to the attenuation of insulin resistance and the activation of hepatic AMPK signalling (Liu et al.2019).
Poisoning by non-edible squash: retrospective series of 353 patients from French Poison Control Centers
Published in Clinical Toxicology, 2018
G. Le Roux, I. Leborgne, M. Labadie, R. Garnier, S. Sinno-Tellier, J. Bloch, M. Deguigne, D. Boels
Consumers seem to be aware of the potential toxicity of colocynths, it is the sudden doubt after ingesting a bitter preparation that motivates the call to the Poison Control Center rather than the symptoms themselves. Cucurbits contain tetracyclic triterpenes called cucurbitacins, mainly in the form of 2-O-beta-glucosides. Based on their chemical structure, these molecules are divided into 12 categories that include cucurbitacins A to T [9]. According to substitutions both on the aglycone portion and the osidic portion, some cucurbitacins (siamenoside I or mogroside IV) are responsible for a sweet taste [1]. Other cucurbitacins were described as bitter molecules. The fruits of bitter cucurbits contain small quantities of cucurbitacin C but large quantities of cucurbitacin E (CucE), which is responsible for the bitter taste [2]. It has been shown that the bitterness of cucurbitacin E is detectable when its concentration reaches 10 ppb (µg/L) in water [10] or as of 2 ppm when it is mixed with pumpkin flesh [2]. Per os, the LD50 values for CucE and its beta-glucoside are 340 and 40 mg/kg, respectively in mice [3]. In rabbits, 2 g/kg of squash is a potentially lethal dose [11]. A 2006 report on the presence of cucurbitacins in vegetables, written at the request of the Danish Council of Ministers, references cases of accidental poisoning by cucurbits containing bitter cucurbitacins. High concentrations of CucE of up to 7.2 g/kg of fresh vegetable have been measured [11], that is, 140 mg in one mouthful of approximately 20 g of puree. Reconciliation of these results confirms the exposure. Even so, the presence of cucurbitacins in patient’s blood cannot be formally linked to a poisoning, in other words, on occurrence of the clinical or biological signs in the patient, who could remain free of symptoms.
The AMPK-SIRT1-FoxO1-NF-κB signaling pathway participates in hesperetin-mediated neuroprotective effects against traumatic brain injury via the NLRP3 inflammasome
Published in Immunopharmacology and Immunotoxicology, 2022
Hai Song, Zhongyun Ding, Jilin Chen, Tingbao Chen, Tinghua Wang, Jin Huang
Vast reports have claimed that AMPK and SIRT1 affect the production of pro-inflammatory cytokines. For example, Mogroside IIIE attenuates high glucose-induced foot cell inflammation and oxidative stress by motivating the AMPK-SIRT1 signaling in diabetic nephropathy [43]. Besides, quercetin heightens the AMPK activity to facilitate SIRT1 expression, thereby down-regulating NF-κB phosphorylation and dampening the production of inflammatory factors and oxidative stressors in endothelial cells in diabetes-induced carotid atherosclerosis [44]. Moreover, the AMPK/SIRT1 pathway activation boosts the expression of anti-inflammatory factors and antioxidant defense-related genes in neurological diseases [45]. For instance, Roflupram ameliorates neuroinflammation by activating the AMPK/SIRT1 pathway to decline LPS-induced IL-6 and TNF-α levels in BV-2 microglia [46]. Dihydromyricetin protects against AD through up-regulation of the AMPK/SIRT1 pathway, thereby suppressing inflammatory responses and hippocampal apoptosis and improving cognitive function [47]. FoxO is an essential autophagy regulator whose activity is mainly regulated by the deacetylation of SIRT1. Multiple reports have indicated that SIRT1 activation exerts anti-oxidative stress, anti-apoptotic and anti-inflammatory properties by deacetylating downstream FoxO1 [48]. NF-κB, known as a transcription factor, activates several genes in the nucleus, including microglial nodd-like receptor protein 3 (NLRP3) [49]. Alterations in FoxO1 activities facilitate NF-κB transcription and thus act on pro-inflammatory cytokines, such as IL-1β and NLRP3, all of which may ameliorate cognitive dysfunction-related disorders [50,51]. However, the function of AMPK-SIRT1-FoxO1-NF-κB in TBI remains unclear. Here, we discovered that phosphorylation of AMPK and SIRT1 was attenuated and phosphorylation of FoxO1-NF-κB and NLRP3 was heightened in damaged brain tissues of TBI mice and OGD/R-treated BV2 microglia, while Hes administration activated the AMPK-SIRT1-FoxO1-NF-κB pathway. These outcomes suggest that Hes relieves neuroinflammation and neuronal apoptosis by activating the SIRT1 AMPK-SIRT1-FoxO1-NF-κB pathway-mediated inflammasomes.