A hybrid algorithm for parameter estimation of the ghrelin dynamics based on in vivo data (CBIC-2017)

Food intake, bodyweight and appetite are controlled by a “web of hormones.”On this work, we shall present a problem in parameter estimation using evolutionary algorithms alongside local search, what we have called hybrid algorithms (global search + local search); furthermore, we apply artificial neural networks (feedforward neural network) for supporting the numerical simulations (what we have called “fake data”). We present a mathematical model for ghrelin partially published elsewhere by the same authors; furthermore, we have confronted the model mathematically with in vivo data via parameter estimation and got promising results for the novel mathematical formulation. Notwithstanding the parameter estimation was unable to model precisely the experimental data, most likely due to physiological details still unclear in the medical literature, it generated an optimized curve relatively close to the experimental data, leaving promising results for future investigations.

Track: Evolutionary, swarm and nature-inspired computation: Real World Applications

See on CBIC: http://cbic2017.org/Evolutionary

Sabor y regulación de la ingestión de alimentos: ensayos y comentarios

Un modelo básico de satisfacción se reduce a sólo dos contribución, dos grupos de señales que se transmiten desde el tracto gastrointestinal al cerebro: 1) estómago y 2) señales y metabolismo intestinal. Recientes investigaciones han dado lugar a una modelo ampliada de la vista clásica, necesaria para modelos más realistas. En este punto de vista, satisfacción intestinal es la suma de no sólo señales relacionadas con valores calóricos de los alimentos, pero también de sustancias no calórico presente en las comidas. En este artículo se describe un artículo publicado recientemente por terceros relacionados con el impacto de "saborizante" (tastants), sustancias sin valores calóricos utilizados ampliamente en la industria como una manera de mejorar los sabores en los alimentos, en la sensación de hambre y el consumo de alimentos. Se une los datos/resultados in vivo (infusión de saborizante directamente en el duodeno) con un modelo en desarrollo por el autor y colaboradores, por lo tanto capaz de replicar parte de los resultados de el artículo citado. El resultado fundamental de este artículo supracitado es el factor fisiológico que los sabores pueden reducir de forma independiente el hambre y la ingesta de alimentos; con un nivel de impacto diferente, umami siendo el más fuerte, y la suma de los sabores siendo incluso más fuerte.

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Sabor e regulação da ingestão de alimentos: ensaios e comentários

Um modelo básico da satisfação se resume a simplesmente dois termos, dois grupos de sinais sendo transmitidos do trato gastrointestinal ao cérebro: 1) estômago e 2) sinais e metabolismo vindos do intestino. Investigações recentes têm propiciado um modelo estendido desta visão clássica, e necessário para modelos mais realísticos. Nesta forma de pensar, satisfação intestinal é a soma não somente de sinais relacionados a valores calóricos do alimento, mas também de substância não-calóricas presente em refeições. Neste artigo, discute-se um artigo publicado recentemente por terceiros relacionado ao impacto de "saborizante" (tastants), substância sem valores calóricos usadas largamente na indústria como forma de reforçar sabores em alimentos, na sensação de fome e consumo de alimentos. Une-se os dados/resultados in vivo (infusões de sabores direto no duodeno) com um modelo em desenvolvimento pelo autor e colaboradores, assim conseguindo-se replicar parte dos resultados do artigo analisado.O resultado-chave do artigo mencionado é o fato fisiológico que sabores conseguem independentemente diminuir fome e consumo de alimentos; com diferente nível de impacto, sendo umami o mais forte, e soma dos sabores ainda mais forte.

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Taste and the regulation of food intake: insights and comments

A modest archetypal of satiation is that it boils down primarily to two categories of signals transmitted from the gastrointestinal tract to the brain: stomach and intestine sensing and metabolism. Novel investigations endow us with the view that an extension of this traditional model is conceivable and called for, wherein intestinal satiation is the byproduct not only from signals related to the caloric content of ingested nutrients, but also from noncaloric properties of ‘tastant molecules’ in foodstuff. On this paper we discuss a recently published paper regarding the impact of tastants (e.g., noncaloric substance widely used as taste enhancers) on hunger and food intake. We gather the in vivo results (nasoduodenal infusions of tastants) with a recently developed mathematical model for ghrelin by the author and co-workers and we successfully replicate in silico part of the findings. The key results from the abovementioned paper and replicated herein is that tastant can inhibit hunger; with different levels of impact, umami being the strongest one, and the union of them being even stronger.

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Mathematical modeling in energy homeostasis, appetite control and food intake with a special attention to ghrelin (PhD thesis)

Notwithstanding considerable variations in daily food intake, animals uphold a remarkably stable body weight, since overall caloric ingestion and expenditure are exquisitely matched over long periods of time, by the process of energy homeostasis.

David E Cummings and Joost Overduin, 2007⁽¹⁵²⁾

The elegant ‘interconnected mechanisms’ by which the gastrointestinal (GI) tract regulates food intake are a marvel of biology, but the redundancy (e.g., several hormones seem to have effects in food intake)  of both GI (by means of hormones) and central nervous system (CNS, by means of satiety/satiation signals) pathways governing energy homeostasis poses formidable challenges for scientists trying to take a clear glimpse of this machinery, e.g. for designing anti-obesity and alike pharmaceuticals.

Some insights into an integrative mathematical model

The ambition of this document is to set in evidence the prerequisite for integrative (mathematical) models, mechanism-based models, for appetite/bodyweight control. For achieving this goal, it is provided a scrutinized literature review and it is organized them in such a way to make the point. The quantitative methods exploited by the authors are called differential equations solved numerically; they are discussed briefly since it is not our goal herein to handle details. On the current state of the art, there is no mathematical model to the best of the author’s knowledge targeting at integrating several hormones at once in mathematical descriptions: even for single hormones, the literature is either occasional or do not exist at all; it is depicted some results for simple models already built. As it can be seen, the functions and roles seem fuzzy, most hormones seem to be piloting the same undertaking. The key challenge from a mathematical modeling perspective is how to separate properly the mechanisms of each hormone. The kind of pursuit presented herein could initiate an imperative cascade of mathematical modeling applied to metabolism of bodyweight control and energy homeostasis.

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Insulin is Required for Prandial Ghrelin Suppression in Humans

Accumulating evidence indicates that ghrelin plays a role in regulating food intake and energy homeostasis. In normal subjects, circulating ghrelin concentrations decrease after meal ingestion and increase progressively before meals. At present, it is not clear whether nutrients suppress the plasma ghrelin concentration directly or indirectly by stimulating insulin secretion. To test the hypothesis that insulin regulates postprandial plasma ghrelin concentrations in humans, we compared the effects of meal ingestion on plasma ghrelin levels in six C-peptide-negative subjects with type 1 diabetes and in six healthy subjects matched for age, sex, and BMI. In conclusion, 1) insulin is essential for meal-induced plasma ghrelin suppression, 2) basal insulin availability is sufficient for postprandial ghrelin suppression in type 1 diabetic subjects, and 3) lack of meal-induced ghrelin suppression caused by severe insulin deficiency may explain hyperphagia of uncontrolled type 1 diabetic subjects.

Full work: http://www.medscape.com/viewarticle/465766.