scholarly journals CD36 Senses Dietary Lipids and Regulates Lipids Homeostasis in the Intestine

2021 ◽  
Vol 12 ◽  
Author(s):  
Lei Zhao ◽  
Yuqi Li ◽  
Qiuying Ding ◽  
Yanping Li ◽  
Yaxi Chen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Scavenger Receptor ◽  
Dietary Lipids ◽  
Intestinal Hormones ◽  
Complex Interactions ◽  
Multiple Ligands ◽  
Proximal Intestine

Dietary lipids absorbed in the intestine are closely related to the development of metabolic syndrome. CD36 is a multi-functional scavenger receptor with multiple ligands, which plays important roles in developing hyperlipidemia, insulin resistance, and metabolic syndrome. In the intestine, CD36 is abundant on the brush border membrane of the enterocytes mainly localized in proximal intestine. This review recapitulates the update and current advances on the importance of intestinal CD36 in sensing dietary lipids and regulating intestinal lipids uptake, synthesis and transport, and regulating intestinal hormones secretion. However, further studies are still needed to demonstrate the complex interactions between intestinal CD36 and dietary lipids, as well as its importance in diet associated metabolic syndrome.

Dietary lipids and gene expression

2004 ◽  
Vol 32 (6) ◽  
pp. 999-1002 ◽  
Author(s):  
H.M. Roche
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Transcription Factors ◽  
Fatty Acid ◽  
Regulatory Element ◽  
Nuclear Factor Κb ◽  
Dietary Lipids ◽  
Dietary Fatty Acids ◽  
Dietary Fatty Acid ◽  
The Metabolic Syndrome

Nutrition is a key environmental factor that is particularly involved in the pathogenesis and progression of several polygenic, diet-related diseases. Nutrigenomics refers to the interaction between nutrition and the human genome. Dietary fatty acids interact with multiple nutrient-sensitive transcription factors. This explains the molecular basis of some of the health effects associated with altered dietary fatty acid composition. The metabolic syndrome is a very common condition, characterized by insulin resistance, abdominal obesity, dyslipidaemia and hypertension. It often precedes Type 2 diabetes mellitus, and is associated with a greater risk of cardiovascular disease. Several lines of evidence suggest that the interaction between nutrient-derived metabolic stressors and pro-inflammatory signals play an important role in the aetiology of insulin resistance and the development of the metabolic syndrome. This paper will address the interaction between several nutrient-sensitive transcription factors, including SREBP (sterol-regulatory-element-binding protein) and NFκB (nuclear factor κB), demonstrating how this interaction may be altered with dietary fatty acid interventions.

scholarly journals Aboral changes in d-glucose transport by human intestinal brush-border membrane vesicles

1986 ◽  
Vol 237 (1) ◽  
pp. 229-234 ◽  
Author(s):  
M K Bluett ◽  
N N Abumrad ◽  
N Arab ◽  
F K Ghishan
Keyword(s):  
Glucose Transport ◽  
Brush Border ◽  
Terminal Ileum ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Intestinal Brush Border Membrane ◽  
Proximal Intestine ◽  
Taurocholate Transport ◽  
Colonic Transport

D-Glucose transport was investigated in isolated brush-border membrane vesicles from human small intestine. Characteristics of D-glucose transport from the jejunum were compared with that in the mid and terminal ileum. Jejunal and mid-ileal D-glucose transport was Na+-dependent and electrogenic. The transient overshoot of jejunal D-glucose transport was significantly greater than corresponding values in mid-ileum. The terminal ileum did not exhibit Na+-dependent D-glucose transport, but did exhibit Na+-dependent taurocholate transport. Na+-glucose co-transport activity as measured by tracer-exchange experiments was greatest in the jejunum, and diminished aborally. We conclude that D-glucose transport in man is Na+-dependent and electrogenic in the proximal intestine and directly related to the activity of D-glucose-Na+ transporters present in the brush-border membranes. D-Glucose transport in the terminal ileum resembles colonic transport of D-glucose.

scholarly journals Glycyl-l-proline transport in rabbit enterocyte basolateral-membrane vesicles

1990 ◽  
Vol 269 (3) ◽  
pp. 565-571 ◽  
Author(s):  
J Dyer ◽  
R B Beechey ◽  
J P Gorvel ◽  
R T Smith ◽  
R Wootton ◽  
...  
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicle ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Peptide Transport ◽  
Marker Enzyme ◽  
Basolateral Membrane Vesicles ◽  
Protein Markers ◽  
Proximal Intestine

The properties of a peptide-transport system in rabbit enterocyte basolateral membrane were examined with glycyl-L-proline as the substrate. Basolateral-membrane vesicles prepared from rabbit proximal intestine were characterized in terms of both purity and orientation. Marker-enzyme assays show that the basolateral-membrane marker, ouabain-sensitive K(+)-activated phosphatase, is enriched 17-fold with respect to the initial homogenate. The activities of enzymes used as markers for other membranes and organelles are low, and contamination of the final membrane fraction with these is minimal. The use of immunoblotting techniques further confirms the absence of brush-border-membrane contamination. Proteins in the basolateral-membrane vesicle preparation gave no cross-reaction with antibodies against the 140 kDa antigen and the Na+/glucose-symport protein, markers specific to the brush-border membrane of the enterocyte. Conversely, antibodies raised against the classical basolateral-membrane marker, the RLA class I histocompatibility complex, reacted strongly with a 43 kDa basolateral-membrane protein. The orientation of the basolateral-membrane vesicles was shown to be predominantly inside-out on determination by two independent criteria. The uptake of [1-14C]glycyl-L-proline by these vesicles is stimulated by the presence of an inwardly directed pH gradient, and this stimulation can be abolished by the proton ionophores carbonyl cyanide p-trichloromethoxyphenylhydrazone (CCCP) and tetrachlorotrifluoromethylbenzimidazole (TTFB). Transport is also inhibited by HgCl2, thimerosal, Na+ and other glycyl dipeptides.

Transport of guanidine in rabbit intestinal brush-border membrane vesicles

1988 ◽  
Vol 255 (1) ◽  
pp. G85-G92 ◽  
Author(s):  
Y. Miyamoto ◽  
V. Ganapathy ◽  
F. H. Leibach
Keyword(s):  
Brush Border ◽  
Time Course ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Extracellular Ph ◽  
Brush Border Membrane Vesicles ◽  
Intestinal Brush Border Membrane ◽  
Intestinal Brush Border ◽  
Dependent Transport ◽  
Proximal Intestine

The characteristics of guanidine uptake were studied in brush-border membrane vesicles isolated from the rabbit proximal intestine. Guanidine uptake was manyfold greater in the presence of an outward-directed H+ gradient (intracellular pH = 5.5; extracellular pH = 7.2) than in the absence of a H+ gradient (intracellular and extracellular pH = 7.2). The time course of guanidine uptake exhibited an overshoot phenomenon in the presence of the H+ gradient, indicating occurrence of uphill transport. This H+ gradient-stimulated guanidine uptake was not due to an inside-negative H+-diffusion potential because carbonyl cyanide 4-trifluoromethoxyphenylhydrazone, a protonophore, failed to have any effect on guanidine uptake. Moreover, the transient uphill transport of guanidine was observed even in voltage-clamped membrane vesicles. However, under the conditions that effectively dissipated the H+ gradient, there was no active transport of guanidine. This H+ gradient-dependent transport mechanism for guanidine is distinct from the Na+-H+ exchanger, because amiloride did not inhibit guanidine uptake even at a concentration as high as 100 microM. These data provide evidence for the presence of a guanidine-H+ antiport system in the rabbit intestinal brush-border membrane. The presence of a carrier for guanidine in these membranes is further substantiated by the trans-stimulation of the uptake of radiolabeled guanidine by unlabeled guanidine and by the inhibition of guanidine uptake by imipramine under equilibrium exchange conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential changes to splanchnic and peripheral protein metabolism during the diet-induced development of metabolic syndrome in rats

2020 ◽  
Vol 319 (1) ◽  
pp. E175-E186
Author(s):  
O. L. Mantha ◽  
J.-F. Huneau ◽  
V. Mathé ◽  
D. Hermier ◽  
N. Khodorova ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Protein Synthesis ◽  
Positive Association ◽  
Dietary Lipids ◽  
Acid Oxidation ◽  
Liver Protein ◽  
High Fat ◽  
Anabolic Resistance ◽  
Protein Mass

Little is known about the effects of the development of metabolic syndrome (MS) on protein and amino acid (AA) metabolism. During this study, we took advantage of the variability in interindividual susceptibility to high fat diet-induced MS to study the relationships between MS, protein synthesis, and AA catabolism in multiple tissues in rats. After 4 mo of high-fat feeding, an MS score (ZMS) was calculated as the average of the z-scores for individual MS components [weight, adiposities, homeostasis model for the assessment of insulin resistance (HOMA-IR), and triglycerides]. In the small intestine, liver, plasma, kidneys, heart, and muscles, tissue protein synthesis was measured by 2H2O labeling, and we evaluated the proportion of tissue AA catabolism (relative to protein synthesis) and nutrient routing to nonindispensable AAs in tissue proteins using natural nitrogen and carbon isotopic distances between tissue proteins and nutrients (Δ15N and Δ13C), respectively. In the liver, protein mass and synthesis increased, whereas the proportion of AA catabolism decreased with ZMS. By contrast, in muscles, we found no association between ZMS and protein mass, protein synthesis (except for a weak positive association in the gastrocnemius muscle only), and proportion of AA catabolism. The development of MS was also associated with altered metabolic flexibility and fatty acid oxidation, as shown by less routing of dietary lipids to nonindispensable AA synthesis in liver and muscle. In conclusion, MS development is associated with a greater gain of both fat and protein masses, with higher protein anabolism that mainly occurs in the liver, whereas muscles probably develop anabolic resistance due to insulin resistance.

Lipid absorptions passing through the unstirred layers, brush-border membrane, and beyond

1993 ◽  
Vol 71 (8) ◽  
pp. 531-555 ◽  
Author(s):  
A. B. R. Thomson ◽  
C. Schoeller ◽  
M. Keelan ◽  
L. Smith ◽  
M. T. Clandinin
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Brush Border ◽  
Binding Proteins ◽  
Brush Border Membrane ◽  
Water Layer ◽  
Lipid Binding ◽  
Dietary Lipids ◽  
Unstirred Water Layer ◽  
Lipid Binding Proteins

Lipids are components of our diet and luminal secretions, with physicochemical characteristics that determine their digestion and absorption in the gastrointestinal tract. Lipids include triglycerides, phospholipids, and cholesterol. Dietary lipids contain approximately 97% triglycerides, with small amounts of phospholipids and cholesterol. These components are important in cell membrane composition, fluidity, peroxidation, prostaglandin and leukotriene synthesis, and cellular metabolic processes. Lipids are implicated in the mechanisms of brain development, inflammatory processes, atherosclerosis, carcinogenesis, aging, and cell renewal. Duodenal hydrolysis of dietary lipids and biliary phospholipids and cholesterol is carried out by pancreatic lipase, colipase, phospholipase A2, and cholesterol esterase. Bile acid solubilization results in mixed micelles and liposomes, in gel and liquid crystal phases. Lipid digestion products pass across the intestinal unstirred water layer. For long-chain fatty acids and cholesterol, passage across the unstirred water layer is rate limiting, whereas passage of short- and medium-chain fatty acids is limited by the brush-border membrane. Within the unstirred water layer, an acidic microclimate aids micellar dissociation so that protonated, and to a lesser extent, nonprotonated monomers then pass across the intestinal brush-border membrane. Absorptive mechanisms have been studied extensively in relation to lipid composition, fatty acid chain length, degree of unsaturation, essential fatty acid content, phospholipid components, and cholesterol. Enterocytes may take up lipids from the intestinal lumen or from lipoproteins of the bloodstream, but these pools are likely to be functionally distinct. Recent advances are reviewed, including recent advances in the area of microclimates, compartmentation, lipid binding proteins, intracellular trafficking, intestinal lipoproteins, release of lipids across the basolateral membrane, and dietary effects.Key words: diet effects, lipid binding proteins, lipoproteins.

Sign in / Sign up

Export Citation Format

Share Document