Effects of acute dietary restriction on gut motor, hormone and energy intake responses to duodenal fat in obese men

Brennan, Ixchel M.; Seimon, Radhika V.; Luscombe-Marsh, Natalie D.; Otto, Barbara; Horowitz, Michael; Feinle‐Bisset, Christine

doi:10.1038/ijo.2010.153

Cited by 27 publications

(26 citation statements)

References 43 publications

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“…On the other hand, it is increased after 4 weeks on a low-fat diet ( 20 ). Similarly, acute dietary restriction in obese subjects enhances gastrointestinal sensitivity to fat, which is associated with an increased effect of fat on satiation ( 45 ). Although we demonstrated the existence of a relationship between fat perception sensitivity and genotype, our study was not able to determine whether oral fat perception sensitivity affects fat intake or body weight.…”

Section: Infl Uence Of Orlistat On Oleic Acid and Triolein Detection contrasting

confidence: 57%

The fatty acid translocase gene CD36 and lingual lipase influence oral sensitivity to fat in obese subjects

Pepino

Love‐Gregory

Klein

et al. 2012

Journal of Lipid Research

248

226

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Obesity is caused by ingesting more energy than is expended over a long period of time. Dietary fat is the most energy-dense macronutrient, and its overconsumption has been linked to obesity ( 1-4 ). Obese people prefer foods with higher fat content ( 5 ), crave high-fat foods more frequently ( 6, 7 ), and consume more fat than lean individuals ( 8 ).Traditionally, perception of fat in the oral cavity is thought to rely almost entirely on textural and aromatic cues activating the somatosensory and olfactory systems. However, there is now increasing evidence to support an important role of the gustatory system in fat perception ( 9-20 ) as well as in intestinal lipid metabolism ( 10, 21 ). Oral and gastrointestinal fat sensory sensitivity appear to be associated ( 16 ) and there is similarity in the chemosensory reception events and their signaling transduction pathways in the tongue and gastrointestinal tract ( 21 ). An important requirement for the involvement of a gustatory component in dietary lipid detection is the hydrolysis of triacylglycerols (TGs) to release free FAs, the signaling stimulus, as was demonstrated through the use of the lipase inhibitor orlistat ( 22 ). In rodents, lingual lipase is essential for the gustatory perception of dietary fats ( 22 ) and the addition of orlistat to fat emulsions diminishes the rat's preference for TG, but not FA ( 22 ). Although it is not known whether lingual lipase is important for oral fat perception in humans, data from a recent study suggests that lingual lipase lipolytic activity can produce FA within the concentration range required to activate oral sensors ( 18 ).Several putative fat taste receptor classes have been identifi ed in rodents ( 12,23,24 ), including the glycoprotein CD36 ( 25 ). The presence of CD36, a scavenger receptor that mediates uptake and traffi cking of lipids in diverse cell types ( 26 ), has been documented in the gustatory papillae of rodents ( 25, 27 ), pigs, and humans ( 28 ). In rodents, the interaction between CD36 and FA results in signaling events that depend on an intact neuronal gustatory pathway ( 15,29 ). CD36 gene knockout impedes fat detection in mice without affecting sweet or bitter perception Abstract The precise orosensory inputs engaged for dietary lipids detection in humans are unknown. We evaluated whether a common single nucleotide polymorphism (rs1761667) in the CD36 gene that reduces CD36 expression and the addition of orlistat, a lipase inhibitor, to reduce FA release from triacylglycerols (TGs), the main component of dietary fats, would attenuate fat orosensory sensitivity in humans. Twenty-one obese subjects with different rs1761667 genotypes (6 AA, 7 AG, and 8 GG) were studied on two occasions in which oleic acid and triolein orosensory detection thresholds were measured using emulsions prepared with and without orlistat. Subjects homozygous for the G-allele had 8-fold lower oral detection thresholds for oleic acid and triolein than subjects homozygous for the A allele, which associates with lower CD36 expr...

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Section: Infl Uence Of Orlistat On Oleic Acid and Triolein Detection contrasting

confidence: 57%

The fatty acid translocase gene CD36 and lingual lipase influence oral sensitivity to fat in obese subjects

Pepino

Love‐Gregory

Klein

et al. 2012

Journal of Lipid Research

248

226

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“…A 30% energy restriction is also concordant with many weight-loss diets. Although fasting ghrelin and hunger ratings were elevated after the dietary restriction, the magnitude of their suppression by intraduodenal lipid was enhanced, and energy intake was markedly reduced (10). In the current study, we observed increased peptide YY and reduced cholecystokinin in response to intraduodenal lipid and an increase in the desire to eat on day 5; however, there were no differences in BPP, IPPWs, antral and duodenal pressures, ghrelin, or energy intakes.…”

Section: Discussioncontrasting

confidence: 62%

“…A silicone-rubber manometry catheter that incorporated 16 channels (Dentsleeve International Ltd) was inserted through an anesthetized nostril into the stomach and allowed to pass into the duodenum by peristalsis (22). Six side holes (channels 1-6) were positioned in the antrum, a 4.5-cm pyloric sleeve sensor (channel 7), with 2 channels present on the back of the sleeve (channels 8 and 9), was positioned across the pylorus, and 7 side holes (channels [10][11][12][13][14][15][16] were positioned in the duodenum. An additional channel, 11.75 cm distal to the pylorus, was used for the intraduodenal infusion.…”

Section: Study Protocolmentioning

confidence: 99%

“…For example, the consumption of a high-fat diet for 14 d accelerated gastric emptying and mouth-to-cecum transit (5) and reduced the pyloric response to intraduodenal lipid (5)(6)(7)(8)(9). Conversely, a 4-d fast slows gastric emptying of glucose in both lean and obese individuals (6) and a 4-d verylow-calorie diet (VLCD) 4 (70% energy restriction; w1000 kcal/d) in obese subjects enhanced the effects of an intraduodenal lipid infusion to stimulate pyloric pressures and plasma peptide YY and suppressed both ghrelin and energy intake (10). Thus, acute energy excess appears to attenuate, and acute severe energy restriction appears to enhance, the gastrointestinal sensitivity to intraduodenal nutrients, particularly lipid.…”

Section: Introductionmentioning

confidence: 99%

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Effects of acute and longer-term dietary restriction on upper gut motility, hormone, appetite, and energy-intake responses to duodenal lipid in lean and obese men

Seimon¹,

Taylor²,

Little³

et al. 2014

The American Journal of Clinical Nutrition

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Background: A 4-d 70% energy restriction enhances gastrointestinal sensitivity to nutrients associated with enhanced energy-intake suppression by lipid. To our knowledge, it is unknown whether these changes occur with 30% energy restriction and are sustained in the longer term. Objectives: We hypothesized that 1) a 4-d 30% energy restriction would enhance effects of intraduodenal lipid on gastrointestinal motility, gut hormones, appetite, and energy intake in lean and obese men and 2) a 12-wk energy restriction associated with weight loss would diminish effects of acute energy restriction on responses to lipid in in obese men. Design: Twelve obese males were studied before (day 0) and after 4 d (day 5), 4 wk (week 4), and 12 wk (week 12), and 12 lean males were studied before and after 4 d of consumption of a 30% energyrestricted diet. On each study day, antropyloroduodenal pressures, gut hormones, and appetite during a 120-min (2.86-kcal/min) intraduodenal lipid infusion and energy intake at a buffet lunch were measured. Results: On day 5, fasting cholecystokinin was less, and ghrelin was higher, in lean (P , 0.05) but not obese men, and lipid-stimulated cholecystokinin and peptide YY and the desire to eat were greater in both groups (P , 0.05), with no differences in energy intakes compared with on day 0. In obese men, a 12-wk energy restriction led to weight loss (9.7 6 0.7 kg). Lipid-induced basal pyloric pressures (BPPs), peptide YY, and the desire to eat were greater (P , 0.05), whereas the amount eaten was less (P , 0.05), at weeks 4 and 12 compared with day 0. Conclusions: A 4-d 30% energy restriction modestly affects responses to intraduodenal lipid in health and obesity but not energy intake, whereas a 12-wk energy restriction, associated with weightloss, enhances lipid-induced BPP and peptide YY and reduces food intake, suggesting that energy restriction increases gastrointestinal sensitivity to lipid. This trial was registered at the Australian New Zealand Clinical Trials Registry (www.anzctr.org.au) as 12609000943246. Am J Clin Nutr 2014;99:24-34.

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“…In general, if these signals change in the obese humans in response to energy-restricted weight loss, a collective signal favoring hunger over satiety/satiation is observed (Table 1). However, detection of this adaptive response is much less consistent than that of circulating adipose signals and nutrients, as they may be dependent on the presence of a negative energy balance (2,30,42,71,133), the amount of weight loss (71), the amount of physical activity (121), the specific derivative of the hormone measured [peptide YY(PYY) vs. PYY3-36; total vs. acetylated ghrelin] (18) or the type of macronutrient restricted in the diet (71,95). Even under the same conditions of weight loss and maintenance, there is a wide variability in individual responses with respect to these adaptations in hunger and satiety signals (18).…”

Section: The Gut: Sensing the Prandial Statementioning

confidence: 99%

Biology's response to dieting: the impetus for weight regain

MacLean

Bergouignan

Cornier

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

370

326

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Dieting is the most common approach to losing weight for the majority of obese and overweight individuals. Restricting intake leads to weight loss in the short term, but, by itself, dieting has a relatively poor success rate for long-term weight reduction. Most obese people eventually regain the weight they have worked so hard to lose. Weight regain has emerged as one of the most significant obstacles for obesity therapeutics, undoubtedly perpetuating the epidemic of excess weight that now affects more than 60% of U.S. adults. In this review, we summarize the evidence of biology's role in the problem of weight regain. Biology's impact is first placed in context with other pressures known to affect body weight. Then, the biological adaptations to an energy-restricted, low-fat diet that are known to occur in the overweight and obese are reviewed, and an integrative picture of energy homeostasis after long-term weight reduction and during weight regain is presented. Finally, a novel model is proposed to explain the persistence of the "energy depletion" signal during the dynamic metabolic state of weight regain, when traditional adiposity signals no longer reflect stored energy in the periphery. The preponderance of evidence would suggest that the biological response to weight loss involves comprehensive, persistent, and redundant adaptations in energy homeostasis and that these adaptations underlie the high recidivism rate in obesity therapeutics. To be successful in the long term, our strategies for preventing weight regain may need to be just as comprehensive, persistent, and redundant, as the biological adaptations they are attempting to counter. energy restriction; diet-induced obesity; obesity prone; weight loss; energy balance IN THE UNITED STATES, OVER 60% of adults and close to 20% of children are overweight or obese (35,174). A number of effective weight loss strategies are available, but most are only transiently effective over a period of 3 to 6 mo. Less than 20% of individuals that have attempted to lose weight are able to achieve and maintain a 10% reduction over a year (128). Over one-third of lost weight tends to return within the first year, and the majority is gained back within 3 to 5 years (3,246). A number of reasons have been proposed for the high incidence of weight regain (69,246), and several point to the biological response to weight loss.The objective of this review is to examine the role of this biological response in the process of weight regain. Biological regulation is first discussed in relation to other nonbiological pressures that affect body weight as weight is gained, lost, and regained. The specific biological adaptations to the most common form of dieting, an energy-restricted low-fat diet, are then discussed in more detail. Previous reviews provide extensive descriptions of the normal adaptive response to energy restriction. We do not attempt to recapitulate those efforts here. Rather, the unique perspective of this review summarizes those adaptations that have been confirmed o...

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Effects of acute dietary restriction on gut motor, hormone and energy intake responses to duodenal fat in obese men

Cited by 27 publications

References 43 publications

The fatty acid translocase gene CD36 and lingual lipase influence oral sensitivity to fat in obese subjects

The fatty acid translocase gene CD36 and lingual lipase influence oral sensitivity to fat in obese subjects

Effects of acute and longer-term dietary restriction on upper gut motility, hormone, appetite, and energy-intake responses to duodenal lipid in lean and obese men

Biology's response to dieting: the impetus for weight regain

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