The ileal brake: A fifteen-year progress report

Citters, G. W. van; Lin, Henry C.

doi:10.1007/s11894-999-0022-6

Cited by 108 publications

(67 citation statements)

References 40 publications

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“…8 These effects have been attributed to the activation of the ileal brake mechanism. 5 Until recently, it was assumed that undigested nutrients reach the distal small intestine only under conditions of malabsorption or maldigestion. A more recent study in dogs has clearly shown that even under physiological circumstances, unabsorbed fat reaches the distal small intestine and activates the ileal brake mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…[2][3][4] This may be achieved by activation of the ileal brake. 5 The ileal brake is the primary inhibitory distal-to-proximal feedback mechanism that controls meal transit through the gastrointestinal tract and is thought to regulate and optimize nutrient digestion and absorption. 5 Several studies have shown that direct delivery of lipids into the ileum delays gastric emptying, 6 prolongs small intestinal transit time 7 and induces satiety.…”

Section: Introductionmentioning

confidence: 99%

“…5 The ileal brake is the primary inhibitory distal-to-proximal feedback mechanism that controls meal transit through the gastrointestinal tract and is thought to regulate and optimize nutrient digestion and absorption. 5 Several studies have shown that direct delivery of lipids into the ileum delays gastric emptying, 6 prolongs small intestinal transit time 7 and induces satiety. 8 Long-chain fatty acids are potent triggers of the ileal brake, 5,7 and several studies have demonstrated that the ileal brake is already activated by small amounts of fat or free fatty acids.…”

Section: Introductionmentioning

confidence: 99%

“…5 Several studies have shown that direct delivery of lipids into the ileum delays gastric emptying, 6 prolongs small intestinal transit time 7 and induces satiety. 8 Long-chain fatty acids are potent triggers of the ileal brake, 5,7 and several studies have demonstrated that the ileal brake is already activated by small amounts of fat or free fatty acids. [9][10][11] However, it is not known whether these small amounts of fat are able to induce satiety and influence food intake.…”

Section: Introductionmentioning

confidence: 99%

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Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

et al. 2008

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Objective: The ileal brake is a feedback mechanism activated by nutrients, especially fat, with marked effects on satiety. The effects of low doses of ileal fat on satiety are largely unknown. We therefore studied the effect of ileal vs oral delivery of low doses of fat on satiety and gut peptide secretion. Design: Randomized, single-blind crossover design. Subjects: Sixteen healthy, normal-weight volunteers (6 male; mean age 26 years, mean body mass index 22.4). Intervention: Participants were intubated with a 290-cm-long nasoileal tube and consumed, on 3 consecutive days, either a liquid breakfast with 3 g fat followed by an ileal placebo infusion at t ¼ 105-150 min (treatment C) or a fat-free liquid breakfast followed by an ileal infusion of either an emulsion of 3 g (treatment I3g) or 9 g (treatment I9g) fat (safflower oil). Measurements: Satiety parameters by visual analog scales and plasma concentrations of CCK and PYY. Results: C significantly increased satiety and CCK secretion compared with the fat-free breakfast. Ileal fat perfusion of both 3 and 9 g (I3g and I9g) significantly increased satiety during and after fat perfusion, without differences in satiety between I3g and I9g. During ileal fat infusion, CCK increased dose dependently, whereas PYY concentrations increased significantly only after 9 g of fat. Secretion of CCK but not of PYY correlated to satiety levels. Conclusion: Postprandial satiety following a liquid breakfast can be effectively and significantly increased by small amounts (as little as 3 g) of fat perfused into the ileum. Ileal fat dose-dependently increased CCK but not PYY secretion. The satiating effect of ileal fat may be partly mediated by CCK.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

et al. 2008

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“…Sixth, the lipids in the GI tract provoked delay in gastric emptying which resulted in increased residence time of the co-administered lipophilic drug in the small intestine. This enabled better dissolution of the drug at the absorptive site and thereby improved the absorption (Citters and Lin 1999).…”

Section: Discussionmentioning

confidence: 99%

Formulation of enrofloxacin SLNs and its pharmacokinetics in emu (Dromaius novaehollandiae) birds

Kumar¹,

Arivuchelvan²,

Jagadeeswaran³

et al. 2014

Appl Nanosci

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The study was conducted to formulate the enrofloxacin solid lipid nanoparticles (SLNs) with sustained release profile and improved pharmacological activity and evaluate the pharmacokinetic behaviour of enrofloxacin SLNs after oral routes of administration in emus. The SLNs were prepared using tripalmitin as lipid carrier, Tween 80 and Span 80 as surfactants and polyvinyl alcohol (PVA) as a stabilizer by a hot homogenization coupled with ultrasonication method. The prepared enrofloxacin SLNs formulations were characterized for further investigation in emu birds. The pharmacokinetics of native enrofloxacin was studied after i.v. and oral bolus administration at 10 mg/kg in emu birds and compared with the disposition kinetics of enrofloxacin SLNs. Enrofloxacin and its metabolite ciprofloxacin in plasma were estimated using HPLC and the pharmacokinetic parameters were calculated by a noncompartmental analysis. The results demonstrated that the particle size, polydispersity index, zeta potential, encapsulation efficiency and loading capacity of the SLNs were 154.72 ± 6.11 nm, 0.42 ± 0.11, -28.83 ± 0.60 mV, 59.66 ± 3.22 and 6.13 ± 0.32 %, respectively. AFM and TEM images showed spherical to circular particles with well-defined periphery. In vitro drug release exhibited biphasic pattern with an initial burst release of 18 % within 2 h followed by sustained release over 96 h. Pharmacokinetic results showed that the t 1/2b , AUC 0-? , V darea /F, MRT and bioavailability were 3.107, 1.894, 1.594, 2.993 and 1.895 times enhanced (p \ 0.01), while CL B and b were significantly (p \ 0.01) decreased by 1.958 and 3.056 times compared to the values of native enrofloxacin administered orally. The ratio of AUC 0-t cipro/AUC 0-t enro after administration of native enrofloxacin and enrofloxacin SLNs was less than 10 %. The t 1/2b and MRT of the metabolite were longer than those of the parent substance. The PK/PD results confirmed that the SLNs extended the enrofloxacin concentration upto 48 h against pathogens susceptible to 0.125 lg/mL in emus. The results indicated that SLNs might be a promising delivery system to prolong and enhance the pharmacological activity of enrofloxacin.

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Fat digestion and absorption: Normal physiology and pathophysiology of malabsorption, including diagnostic testing

Omer,

Chiodi

2024

Nut in Clin Prac

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Fat digestion and absorption play crucial roles in maintaining energy homeostasis and supporting essential physiological functions. The initial stage of fat digestion occurs in the stomach, where gastric lipase begins the hydrolysis of triglycerides. However, most fat digestion takes place in the small intestine via pancreatic enzymes and bile salts. Emulsification of fat by bile acids facilitates enzymatic action, breaking down triglycerides into free fatty acids and monoglycerides, which are then able to be absorbed by enterocytes. Fat malabsorption can result from various underlying conditions, such as exocrine pancreatic insufficiency, bile acid disorders, or intestinal diseases. The clinical manifestations of fat malabsorption include steatorrhea, malnutrition, and deficiencies of fat‐soluble vitamins. Diagnostic approaches involve assessing fecal fat levels, imaging studies, and various functional tests to identify the specific etiology. This review article will describe the normal physiologic process of fat digestion and absorption and discuss various pathophysiology that can lead to fat malabsorption within the gastrointestinal tract as well as their respective diagnostic testing modalities. Effective digestion of fat is essential for overall health, because it allows for absorption of many essential nutrients, plays an integral role in cellular and structural function, and supplies energy to the body. When this is dysfunctional, disorders of malabsorption can occur. This article will give a brief overview of the physiologic process of fat digestion and absorption in healthy individuals as well as review important pathophysiology that can lead to fat malabsorption within the gastrointestinal tract and current diagnostic testing modalities.

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The ileal brake: A fifteen-year progress report

Cited by 108 publications

References 40 publications

Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

Formulation of enrofloxacin SLNs and its pharmacokinetics in emu (Dromaius novaehollandiae) birds

Fat digestion and absorption: Normal physiology and pathophysiology of malabsorption, including diagnostic testing

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