Subchronic treatment with grape-seed phenolics inhibits ghrelin production despite a short-term stimulation of ghrelin secretion produced by bitter-sensing flavanols
Abstract:The sustained satiating effects of GSPE are related to a long-term decrease in ghrelin expression. GA and oligomeric flavanols play a ghrelin-inhibiting role in this process.
“…5 However, other effects might be mediated through interactions with the gastrointestinal tract where they act by inhibiting enzymes, 6 modulating inflammation and/or gut barrier properties, 7 or modulating enteroendocrine secretion. 8,9 The effects of flavonoids on gut microbiota have been recently reviewed; 7 but there are few studies analyzing the role of proanthocyanidins on gut microbiota which could also mediate their physiological effects.…”
Section: Introductionmentioning
confidence: 99%
“…Interestingly this treatment also increased energy expenditure, which together with reduced food intake led to a lower body weight gain. 8 The increased satiety has been linked to ghrelin secretion modulation, but whether other enterohomones are regulated in this specific treatment has not been shown. These results point out GSPE as an interesting candidate for ameliorating obesity and diabetes.…”
Grape seed proanthocyanidin extract (GSPE) modulates several parameters involved in metabolic syndrome. GSPE is a mixture of compounds, some which are rapidly absorbed, while others remain in the lumen where they might have effects that are translated to the whole organism. Our aim was to decipher if the 8-day treatment of GSPE, previously shown to reduce food intake, induces changes in the microbiota and enterohormone secretion. The ratio of Firmicutes : Bacteroidetes was lower in the microbiota of GSPE-treated rats compared to controls, and differences in several taxonomic families and genera were observed. Such modulation led to a reduction in cecal butyrate content. GSPE also increased plasma glucagon-like-peptide-1 (GLP-1). Gallic acid did not induce major changes in the microbiota profile nor in GLP-1 secretion. Correlations between several microbiota taxa and plasma triacylglycerol, adiposity, and enterohormones were observed. Modulation of microbiota may be one of the mechanism by which GSPE impacts metabolic health.
“…5 However, other effects might be mediated through interactions with the gastrointestinal tract where they act by inhibiting enzymes, 6 modulating inflammation and/or gut barrier properties, 7 or modulating enteroendocrine secretion. 8,9 The effects of flavonoids on gut microbiota have been recently reviewed; 7 but there are few studies analyzing the role of proanthocyanidins on gut microbiota which could also mediate their physiological effects.…”
Section: Introductionmentioning
confidence: 99%
“…Interestingly this treatment also increased energy expenditure, which together with reduced food intake led to a lower body weight gain. 8 The increased satiety has been linked to ghrelin secretion modulation, but whether other enterohomones are regulated in this specific treatment has not been shown. These results point out GSPE as an interesting candidate for ameliorating obesity and diabetes.…”
Grape seed proanthocyanidin extract (GSPE) modulates several parameters involved in metabolic syndrome. GSPE is a mixture of compounds, some which are rapidly absorbed, while others remain in the lumen where they might have effects that are translated to the whole organism. Our aim was to decipher if the 8-day treatment of GSPE, previously shown to reduce food intake, induces changes in the microbiota and enterohormone secretion. The ratio of Firmicutes : Bacteroidetes was lower in the microbiota of GSPE-treated rats compared to controls, and differences in several taxonomic families and genera were observed. Such modulation led to a reduction in cecal butyrate content. GSPE also increased plasma glucagon-like-peptide-1 (GLP-1). Gallic acid did not induce major changes in the microbiota profile nor in GLP-1 secretion. Correlations between several microbiota taxa and plasma triacylglycerol, adiposity, and enterohormones were observed. Modulation of microbiota may be one of the mechanism by which GSPE impacts metabolic health.
“…We ruled out the possibility that proanthocyanidins were playing an important role in inhibiting the gastrointestinal digestion process [14]. Remarkably, the animals ingested less food, which could be due to the changes induced by the extract on enteroendocrine signals (increased active GLP-1 [17] and decreased acylated ghrelin [18]) and/or by other signals that limit their need to feeding [17]. Bao et al, working with GSPE in diabetic rats and at doses similar to ours, also found an inhibition in food intake after chronic administration [19].…”
Food intake depends on homeostatic and non-homeostatic factors. In order to use grape seed proanthocyanidins (GSPE) as food intake limiting agents, it is important to define the key characteristics of their bioactivity within this complex function. We treated rats with acute and chronic treatments of GSPE at different doses to identify the importance of eating patterns and GSPE dose and the mechanistic aspects of GSPE. GSPE-induced food intake inhibition must be reproduced under non-stressful conditions and with a stable and synchronized feeding pattern. A minimum dose of around 350 mg GSPE/kg body weight (BW) is needed. GSPE components act by activating the Glucagon-like peptide-1 (GLP-1) receptor because their effect is blocked by Exendin 9-39. GSPE in turn acts on the hypothalamic center of food intake control probably because of increased GLP-1 production in the intestine. To conclude, GSPE inhibits food intake through GLP-1 signaling, but it needs to be dosed under optimal conditions to exert this effect.
“…Indeed, as might be assumed, infused mice exhibit increased food consumption for 30 min after the treatment. 71 A number of human studies also reported differential effects of gastric stimulation by different bitter compounds. 69 Delayed gastric emptying, as well as the induction of conditioned taste aversion, has been observed after gastric denatonium benzoate infusion in rats, although blood hormone levels were not monitored in this study.…”
Section: Stomachmentioning
confidence: 99%
“…70 Another study in rats reported differential effects on ghrelin secretion depending on the duration (acute/ chronic) and type of bitter compound used, suggesting the existence of complex activity patterns between receptive molecules and bitter chemicals. 71 A number of human studies also reported differential effects of gastric stimulation by different bitter compounds.…”
The sense of taste is positioned at the forefront when it comes to the interaction of our body with foodborne chemicals. However, the role of our taste system, and in particular its associated taste receptors, is not limited to driving food preferences leading to ingestion or rejection before other organs take over responsibility for nutrient digestion, absorption and metabolic regulation. Taste sensory elements do much more. On the one hand, extra‐oral taste receptors from the brain to the gut continue to sense nutrients and noxious substances after ingestion and, on the other hand, the nutritional state feeds back on the taste system. This intricate regulatory network is orchestrated by endocrine factors that are secreted in response to taste receptor signalling and, in turn regulate the taste receptor cells themselves. The present review summarises current knowledge on the endocrine regulation of the taste perceptual system and the release of hunger/satiety regulating factors by gastrointestinal taste receptors. Furthermore, the regulation of blood glucose levels via the activation of pancreatic sweet taste receptors and subsequent insulin secretion, as well as the influence of bitter compounds on thyroid hormone release, is addressed. Finally, the central effects of tastants are discussed briefly.
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