Augmented capacity for peripheral serotonin release in human obesity

Young, Richard L.; Lumsden, Amanda L.; Martin, Alyce M.; Schober, Gudrun; Pezos, Nektaria; Thazhath, Sony S.; Isaacs, Nicole J.; Cvijanovic, Nada; Sun, Emily; Wu, Tongzhi; Rayner, Christopher K.; Nguyen, Nam Q.; Fontgalland, Dayan de; Rabbitt, Philippa; Hollington, Paul; Sposato, Luigi; Due, Steven L.; Wattchow, David; Liou, Alice P.; Jackson, V. Margaret; Keating, Damien J.

doi:10.1038/s41366-018-0047-8

Cited by 69 publications

(67 citation statements)

References 41 publications

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“…However, it is necessary to be cautious with this upregulation of incretins in response to high-sugar diets, because it has been described that in diabetic patients, who have increased levels of incretins, a reduced incretin effect is observed, which suggest the development of an "incretin resistance" process [280][281][282][283].…”

Section: Impact Of Excessive Dietary Sugars Consumption On Incretin Smentioning

confidence: 99%

Intestinal Fructose and Glucose Metabolism in Health and Disease

et al. 2019

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The worldwide epidemics of obesity and diabetes have been linked to increased sugar consumption in humans. Here, we review fructose and glucose metabolism, as well as potential molecular mechanisms by which excessive sugar consumption is associated to metabolic diseases and insulin resistance in humans. To this end, we focus on understanding molecular and cellular mechanisms of fructose and glucose transport and sensing in the intestine, the intracellular signaling effects of dietary sugar metabolism, and its impact on glucose homeostasis in health and disease. Finally, the peripheral and central effects of dietary sugars on the gut-brain axis will be reviewed.

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Section: Impact Of Excessive Dietary Sugars Consumption On Incretin Smentioning

confidence: 99%

Intestinal Fructose and Glucose Metabolism in Health and Disease

et al. 2019

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“…During early stage of T2D, the intestinal genetic expressions of SGLT1 and GLUT2 are increased in rodents and humans as well as the secretions of intestinal neurohormones in response to glucose in prediabetic rat [8][9][10]. However, these compensatory mechanisms decrease with the diabetes duration in rodents suggesting a development of glucose resistance over time [11,12]. During T2D, the neurohormone blood levels are particularly altered: the concentrations of GLP-1, GIP and 5-HT are maintained high revealing a resistance to the intestinal neuro-hormones as Bincretin resistance^ [12][13][14][15].…”

Section: Glucose-induced Intestinal Neuro-hormone Secretionsmentioning

confidence: 99%

“…However, these compensatory mechanisms decrease with the diabetes duration in rodents suggesting a development of glucose resistance over time [11,12]. During T2D, the neurohormone blood levels are particularly altered: the concentrations of GLP-1, GIP and 5-HT are maintained high revealing a resistance to the intestinal neuro-hormones as Bincretin resistance^ [12][13][14][15].…”

Section: Glucose-induced Intestinal Neuro-hormone Secretionsmentioning

confidence: 99%

The gut microbiota to the brain axis in the metabolic control

Grasset

Burcelin

2019

Rev Endocr Metab Disord

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The regulation of glycemia is under a tight neuronal detection of glucose levels performed by the gut-brain axis and an efficient efferent neuronal message sent to the peripheral organs, as the pancreas to induce insulin and inhibit glucagon secretions. The neuronal detection of glucose levels is performed by the autonomic nervous system including the enteric nervous system and the vagus nerve innervating the gastro-intestinal tractus, from the mouth to the anus. A dysregulation of this detection leads to the one of the most important current health issue around the world i.e. diabetes mellitus. Furthemore, the consequences of diabetes mellitus on neuronal homeostasis and activities participate to the aggravation of the disease establishing a viscious circle. Prokaryotic cells as bacteria, reside in our gut. The strong relationship between prokaryotic cells and our eukaryotic cells has been established long ago, and prokaryotic and eukaryotic cells in our body have evolved synbiotically. For the last decades, studies demonstrated the critical role of the gut microbiota on the metabolic control and how its shift can induce diseases such as diabetes. Despite an important increase of knowledge, few is known about 1) how the gut microbiota influences the neuronal detection of glucose and 2) how the diabetes mellitus-induced gut microbiota shift observed participates to the alterations of autonomic nervous system and the gut-brain axis activity.

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“…Optimally such foods should not be consumed by people at risk of diabetes, but the reality is that individuals continue to consume sweet foods so alternative strategies are necessary. Non-caloric sweeteners are currently under scrutiny because of their association with type 2 diabetes [1] and with enhanced glucose absorption in healthy volunteers [20]. In this study, we aimed to assess the metabolic responses to muffins containing sucrose or fructose before and after a one-month chronic consumption period in which muffins are added to the normal diet.…”

Section: Introductionmentioning

confidence: 99%

Acute Effect of Moderate Dose Fructose in Solid Foods on Triglyceride, Glucose and Uric Acid before and after a One-Month Moderate Sugar Feeding Period - A Randomised Controlled Trial

Clifton¹,

Keogh²

2020

Preprint

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Fructose in beverages has adverse effects on lipids, glucose and insulin sensitivity after acute and chronic ingestion. There is limited data showing that chronic consumption of fructose in solid foods has harmful effects. We hypothesized that a moderate amount of fructose compared with sucrose in solid food consumed for a month would not adversely influence fasting or postprandial lipids and glucose after an acute fat and carbohydrate load. Twenty-five men and women with prediabetes and/or obesity and overweight consumed in random order two acute test meals of muffins sweetened with either fructose or sucrose, followed by 4-week chronic consumption of 42g/day of either fructose or sucrose in low fat muffins after which the 2 meal tests were repeated. Subjects were randomised to sugar type in the chronic feeding period. Sugar type had no effect on the incremental area under the curve for triglyceride or uric acid at either time point (P=0.4 and P=0.9). There was no overall difference between meal tests at baseline and after 1 month and no effect of consuming sucrose or fructose muffins for 1 month. Fasting triglyceride increased after chronic consumption of fructose by 0.31±0.37 mmol/L compared with sucrose in people with IFG/IGT only (P=0.004). Fructose at a moderate intake of <10% of energy in solid food has no different effects on postprandial triglyceride and uric acid compared with sucrose although fasting triglyceride was increased in people with IFG/IGT after 1 month of fructose muffins suggesting the need for caution.

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Augmented capacity for peripheral serotonin release in human obesity

Abstract: Human obesity is characterized by an increased capacity to produce and release 5-HT from the proximal small intestine, which is strongly linked to higher body mass, and glycemic control. Gut-derived 5-HT is likely to be an important driver of pathogenesis in human obesity and dysglycemia.

Cited by 69 publications

References 41 publications

Intestinal Fructose and Glucose Metabolism in Health and Disease

Intestinal Fructose and Glucose Metabolism in Health and Disease

The gut microbiota to the brain axis in the metabolic control

Acute Effect of Moderate Dose Fructose in Solid Foods on Triglyceride, Glucose and Uric Acid before and after a One-Month Moderate Sugar Feeding Period - A Randomised Controlled Trial

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