Brain Feeding Circuits after Roux-en-Y Gastric Bypass

Hankir, Mohammed K.; Seyfried, Florian; Miras, Alexander D.; Cowley, Michael A.

doi:10.1016/j.tem.2018.01.009

Cited by 30 publications

(20 citation statements)

References 125 publications

(220 reference statements)

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“…The central nervous system, especially the hypothalamus, can control the central and peripheral energy homeostasis through neuropeptides and neurotransmitters [59]. Some studies have confirmed that changes in the nervous system can be significantly observed after RYGB [60][61][62]. Liver fat metabolism is regulated by not only humoral but also the nervous system.…”

Section: Discussionmentioning

confidence: 99%

Roux-en-Y Gastric Bypass in Obese Diabetic Rats Promotes Autophagy to Improve Lipid Metabolism through mTOR/p70S6K Signaling Pathway

Tang

et al. 2020

Journal of Diabetes Research

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Purpose. To investigate the effects of Roux-en-Y gastric bypass (RYGB) surgery on markers of liver mitochondrial dynamics and find new therapeutic basis on obese type 2 diabetes mellitus (T2DM) patients. Materials and Methods. Thirty-two rats were divided into nondiabetic group, diabetic group, sham group, and RYGB group. The Dual-energy X-ray absorptiometry (DEXA) was used to detect short-term curriculum vitae for rat body component and fat and lean mass. Hepatic lipid content and triglyceride levels were detected by Oil Red O staining. Western blotting was used to examine autophagy and mammalian target of rapamycin/P70S6 kinase (mTOR/p70S6K) pathway-related proteins. The carbon dioxide production from the oxidation of [14C] oleate was measured. Plasma glucose was measured by glucose oxidase assay. The insulin and C-peptide were detected. Triacylglyceride (TG) and free fat acid (FFA) in plasma were determined by enzymatic colorimetric assays. Results. RYGB improved metabolic parameters and enhanced plasma GLP-1 level, ameliorated the lipopexia, and increased insulin sensitivity in the liver; RYGB promoted the hepatic autophagy and inhibited the mTOR/p70S6K signaling pathway. GLP-1 reduced fat load and increased fatty acid β-oxidation by activated autophagy to regulate the hepatic lipid pathway through mTOR/p70S6K signaling pathway. Conclusions. RYGB may reduce liver lipid toxicity and improve insulin sensitivity through activating the hepatic fat hydrolysis pathway and inhibiting the liver fat synthesis pathway. However, the transport pathway of liver fat does not play a key role.

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Section: Discussionmentioning

confidence: 99%

Roux-en-Y Gastric Bypass in Obese Diabetic Rats Promotes Autophagy to Improve Lipid Metabolism through mTOR/p70S6K Signaling Pathway

Tang

et al. 2020

Journal of Diabetes Research

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“…To conclude this section on interventional strategies, it is interesting to evoke what is still one of the most effective therapeutic compromises against morbid obesity: the Roux-en-Y gastric bypass (RYGB; Kang and Le, 2017). A recent paper reviewed the evidences derived from neuroimaging and animal (mainly rodent) studies (Hankir et al, 2018), explaining how a metabolic surgical procedure such as the RYGB, which is drastically reorganizing gut, including peptide hormones and microbiota metabolites, is also reshaping homeostatic and hedonic brain processes. Different animal models of bariatric surgery have been described (Rao et al, 2010), and the first demonstrations of RYGB in the pig model, to our knowledge, date back to the 1990s (Frantzides et al, 1995;Potvin et al, 1997).…”

Section: Impact Of Bariatric Surgery On Brain Activitymentioning

confidence: 99%

Review: Impact of food, gut–brain signals and metabolic status on brain activity in the pig model: 10 years of nutrition research using in vivo brain imaging

Val‐Laillet

2019

Animal

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The purpose of this review is to offer a panorama on 10 years of nutrition research using in vivo brain imaging in the pig model. First, we will review some work describing the brain responses to food signals, including basic tastants such as sweet and bitter at both oral and visceral levels, as well as conditioned preferred and aversive flavours. Second, we will have a look at the impact of weight gain and obesity on brain metabolism and functional responses, drawing the parallel with obese human patients. Third, we will evoke the concept of the developmental origins of health and diseases, and how the pig model can shed light on the importance of maternal nutrition during gestation and lactation for the development of the gut-brain axis and adaptation abilities of the progeny to nutritional environments. Finally, three examples of preventive or therapeutic strategies will be introduced: the use of sensory food ingredients or pre-, pro-, and postbiotics to improve metabolic and cognitive functions; the implementation of chronic vagus nerve stimulation to prevent weight gain and glucose metabolism alterations; and the development of bariatric surgery in the pig model for the understanding of its complex mechanisms at the gut-brain level. A critical conclusion will brush the limitations of neurocognitive studies in the pig model and put in perspective the rationale and ethical concerns underlying the use of pig experimentation in nutrition and neurosciences. ImplicationsThe purpose of this review is to offer a panorama on 10 years of nutrition research using in vivo brain imaging in the pig model, and to improve the understanding of the gut-brain axis factors modulating brain activity. This research has implications in the context of animal and human nutrition and health, covering the scope of animal production as well as translational medicine. In addition to the original insight these provide in neurocognitive and developmental sciences, the scientific studies presented here are valuable for the development of new preventive, diagnosis and therapeutics solutions to fight against nutritional and behavioural disorders.

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“…An early demonstration of neural regulation of insulin release was in rats fed sham meals, or entrained to stimuli related to eating. 9,[12][13][14] It is clear that GB has substantial effects on brain centres controlling feeding behaviour 15 ; thus, it is plausible that the CNS also affects islet hormone release after surgery. 10,12 Both cephalic 11 and prandial 10 insulin secretion is mediated in great part by parasympathetic stimuli carried in the vagus nerve.…”

Section: Introductionmentioning

confidence: 99%

“…10,12 Both cephalic 11 and prandial 10 insulin secretion is mediated in great part by parasympathetic stimuli carried in the vagus nerve. 9,[12][13][14] It is clear that GB has substantial effects on brain centres controlling feeding behaviour 15 ; thus, it is plausible that the CNS also affects islet hormone release after surgery.…”

mentioning

confidence: 99%

Role of vagal activation in postprandial glucose metabolism after gastric bypass in individuals with and without hypoglycaemia

Salehi

Gastaldelli

D’Alessio

2019

Diabetes Obesity Metabolism

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Patients who have undergone gastric bypass surgery (GB) have enhanced postprandial hyperinsulinaemia and a greater incretin effect is apparent. In the present study, we sought to determine the effect of vagal activation, a neural component of the enteroinsular axis, on postprandial glucose metabolism in patients with and without hypoglycaemia after GB. Seven patients with documented post-GB hypoglycaemia, seven asymptomatic patients without hypoglycaemia post-GB, and 10 weight-matched non-surgical controls with normal glucose tolerance were recruited. Blood glucose, and islet hormone and incretin secretion were compared during mixed meal tolerance tests (MMTs) with and without prior sham-feeding on two separate days.Sham feeding preceding the MMT caused a more rapid increase in prandial blood glucose levels but lowered overall glycaemia in all three groups (P < 0.05). Sham feeding had a similar effect to increase early (P < 0.05), but not overall, meal-induced insulin secretion in the three groups.Prandial glucagon concentrations were significantly greater in the GB groups, and sham feeding accentuated this response (P < 0.05). The effect of vagal activation on prandial glucose and islet-cell function is preserved in patients who have undergone GB, in those both with and without hypoglycaemia. K E Y W O R D Sβ-cell function, bariatric surgery, hypoglycaemia, incretin physiology

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Brain Feeding Circuits after Roux-en-Y Gastric Bypass

Cited by 30 publications

References 125 publications

Roux-en-Y Gastric Bypass in Obese Diabetic Rats Promotes Autophagy to Improve Lipid Metabolism through mTOR/p70S6K Signaling Pathway

Roux-en-Y Gastric Bypass in Obese Diabetic Rats Promotes Autophagy to Improve Lipid Metabolism through mTOR/p70S6K Signaling Pathway

Review: Impact of food, gut–brain signals and metabolic status on brain activity in the pig model: 10 years of nutrition research using in vivo brain imaging

Role of vagal activation in postprandial glucose metabolism after gastric bypass in individuals with and without hypoglycaemia

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