Overeating makes the gut grow fonder; new insights in gastrointestinal satiety signaling in obesity

Maljaars, Jeroen

doi:10.1097/mog.0b013e32835d9fe0

Cited by 7 publications

(4 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This pattern could be due to the fact that a particular increase in caloric intake is likely to sustain a larger body weight increase in persons with higher adiposity . It could also be due to disruptions in gut peptide signaling leading to attenuated satiety in persons with diet‐induced obesity .…”

Section: Discussionmentioning

confidence: 99%

Chocolate‐candy consumption and 3‐year weight gain among postmenopausal U.S. women

Greenberg

Manson

Buijsse

et al. 2015

Obesity

View full text Add to dashboard Cite

OBJECTIVE To test the hypothesis that greater chocolate-candy intake is associated with more weight gain in postmenopausal women. DESIGN AND METHODS Prospective cohort study involving 107,243 post-menopausal American women aged 50–79 years (mean=60.7) at enrolment in the Women’s Health Initiative (WHI), with three-year follow up. Chocolate-candy consumption was assessed by food frequency questionnaire and body weight was measured. Linear mixed models, adjusted for demographic, socio-economic, anthropomorphic and behavioral variables, were used to test our main hypotheses. RESULTS Compared to women who ate a 1 oz (~28 g) serving of chocolate candy <1 per month, those who ate this amount 1 per month to <1 per week, 1 per week to < 3 per week and ≥3 per week showed greater three-year prospective weight gains (kg) of 0.76 (95% CI: 0.66, 0.85), 0.95 (0.84, 1.06) and 1.40 (1.27, 1.53), respectively, (p for linear trend<0.0001). Each additional 1 oz/day was associated with a greater three-year weight gain (kg) of 0.92 (0.80, 1.05). The weight gain in each chocolate-candy intake level increased as BMI increased above the normal range (18.5–25 kg/m2), and as age decreased. CONCLUSIONS Greater chocolate-candy intake was associated with greater prospective weight gain in this cohort of post-menopausal women.

show abstract

Section: Discussionmentioning

confidence: 99%

Chocolate‐candy consumption and 3‐year weight gain among postmenopausal U.S. women

Greenberg

Manson

Buijsse

et al. 2015

Obesity

View full text Add to dashboard Cite

show abstract

“…In obesity, impairment in gastrointestinal responses to nutrients and subsequent gut peptide secretion may be at least partially responsible for decreased satiety and increased energy intake [14]. Consistent with this idea, postprandial plasma levels of CCK and PYY were found to be reduced in obese human subjects, relative to lean controls [15].…”

Section: Introductionmentioning

confidence: 94%

Feeding-induced oleoylethanolamide mobilization is disrupted in the gut of diet-induced obese rodents

Igarashi

DiPatrizio

Narayanaswami

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

View full text Add to dashboard Cite

The gastrointestinal tract plays a critical role in the regulation of energy homeostasis by initiating neural and hormonal responses to the ingestion of nutrients. In addition to peptide hormones, such as cholecystokinin (CKK) and peptide YY (PYY), the lipid-derived mediator oleoylethanolamide (OEA) has been implicated in the control of satiety. Previous studies in humans and rodent models have shown that obesity is associated with changes in CCK, PYY and other gut-derived peptide hormones, which may contribute to decreased satiety and increased energy intake. In the present study, we show that small-intestinal OEA production is disrupted in the gut of diet-induced obese (DIO) rats and mice. In lean rodents, feeding or duodenal infusion of Intralipid® or pure oleic acid stimulate jejunal OEA mobilization. This response is strikingly absent in DIO rats and mice. Confirming previous reports, we found that feeding rats or mice a high-fat diet for 7 days is sufficient to suppress jejunal OEA mobilization. Surprisingly, a similar effect is elicited by feeding rats and mice a high-sucrose low-fat diet for 7 days. Collectively, our findings suggest that high fat-induced obesity is accompanied by alterations in the post-digestive machinery responsible for OEA biosynthesis, which may contribute to reduced satiety and hyperphagia.

show abstract

“…Thus, in this study, the effects of intraduodenal infusion of fat and CHO on food intake and satiety were not affected by BMI. In addition, Maljaars, et al described altered gut peptide secretion and blunted vagal responses to nutrients when obesity develops [ 62 ]. Thus, it can be suggested that obesity leads to altered gastrointestinal responses to nutrients.…”

Section: The Effect Of Bmi Age and Gender On The Intestinal Brakmentioning

confidence: 99%

Gastrointestinal Nutrient Infusion Site and Eating Behavior: Evidence for A Proximal to Distal Gradient within the Small Intestine?

et al. 2016

View full text Add to dashboard Cite

The rapidly increasing prevalence of overweight and obesity demands new strategies focusing on prevention and treatment of this significant health care problem. In the search for new and effective therapeutic modalities for overweight subjects, the gastrointestinal (GI) tract is increasingly considered as an attractive target for medical and food-based strategies. The entry of nutrients into the small intestine activates so-called intestinal “brakes”, negative feedback mechanisms that influence not only functions of more proximal parts of the GI tract but also satiety and food intake. Recent evidence suggests that all three macronutrients (protein, fat, and carbohydrates) are able to activate the intestinal brake, although to a different extent and by different mechanisms of action. This review provides a detailed overview of the current evidence for intestinal brake activation of the three macronutrients and their effects on GI function, satiety, and food intake. In addition, these effects appear to depend on region and length of infusion in the small intestine. A recommendation for a therapeutic approach is provided, based on the observed differences between intestinal brake activation.

show abstract

Overeating makes the gut grow fonder; new insights in gastrointestinal satiety signaling in obesity

Abstract: DIO alters nutrient-induced gastrointestinal signaling in a way that facilitates further weight gain and complicates weight loss. A better understanding of these mechanisms and the way bariatric surgery can overcome these changes is crucial in developing effective treatment strategies.

Cited by 7 publications

References 46 publications

Chocolate‐candy consumption and 3‐year weight gain among postmenopausal U.S. women

Chocolate‐candy consumption and 3‐year weight gain among postmenopausal U.S. women

Feeding-induced oleoylethanolamide mobilization is disrupted in the gut of diet-induced obese rodents

Gastrointestinal Nutrient Infusion Site and Eating Behavior: Evidence for A Proximal to Distal Gradient within the Small Intestine?

Contact Info

Product

Resources

About