Responses of celiac and cervical vagal afferents to infusions of lipids in the jejunum or ileum of the rat

2000 ◽  
Vol 278 (1) ◽  
pp. R34-R43 ◽  
Author(s):  
Alan Randich ◽  
William J. Tyler ◽  
James E. Cox ◽  
Stephen T. Meller ◽  
Gary R. Kelm ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Linoleic Acid ◽  
Single Unit ◽  
Corn Oil ◽  
Body Weight Gain ◽  
Vagal Afferents ◽  
Afferent Activity ◽  
Inhibitory Effects ◽  
Vagal Afferent ◽  
Increased Activity

Multiunit celiac and single-unit cervical recordings of vagal afferents were performed before and during infusions of fatty acids, triglycerides, or saline into either the ileum or jejunum of the rat. In multiunit recordings, lipids increased activity of vagal afferents to a greater extent than saline. The greatest increases in vagal afferent activity resulted from infusions of linoleic acid, conjugated linoleic acid, or oleic acid. The triglycerides, corn oil or Intralipid, were less effective than the fatty acids in affecting vagal afferent activity. Ileal pretreatment with the hydrophobic surfactant Pluronic L-81 significantly attenuated the response of celiac vagal afferents to ileal infusion of linoleic acid. Single-unit recordings of cervical vagal afferents supported the multiunit data in showing lipid-induced increased vagal afferent activity in ∼50% of ileal units sampled and 100% of a limited number of jejunal units sampled. These data demonstrate that free fatty acids can activate ileal and jejunal vagal afferents in the rat, and this effect can be attenuated by pretreatment with a chylomicron inhibitor. These data are consistent with the view that lipid-induced activation of vagal afferents could be a potential substrate for the inhibitory effects of intestinal lipids on gastrointestinal function, food intake, and body weight gain.

scholarly journals CONTENT OF FATTY ACIDS IN CORN (ZEA MAYS L.) OIL FROM ECUADOR

2017 ◽  
Vol 10 (8) ◽  
pp. 150 ◽  
Author(s):  
Carrillo W ◽  
Carpio C ◽  
Morales D ◽  
Vilcacundo E ◽  
Álvarez M ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Zea Mays ◽  
Oleic Acid ◽  
Linoleic Acid ◽  
Corn Oil ◽  
Methyl Esters ◽  
Total Content ◽  
Pressing Method ◽  
A Value ◽  
Omega 6

  Objective: The aim of this work was to determine the fatty acids content in corn seeds oil (Zea mays) sample cultivated in Ecuador.Methods: Corn oil was obtained from corn oil seeds using the cold pressing method. Methyl esters fatty acids analysis were carried out using the gas chromatography (GC) method with a mass selective detector and using the database library NIST 14.L to identify the compounds present in the corn seed oil.Results: Methyl esters fatty acids were identified from corn (Z. mays) seeds using the GC mass spectrometer (GC-MS) analytical method. Fatty acids were analyzed as methyl esters on a capillary column DB-WAX 122-7062 with a good separation of palmitic acid, stearic acid, oleic acid, elaidic acid, linoleic acid, arachidic acid, and linolenic acid. The structure of methyl esters fatty acids was determined using the GS-MS method. Corn oil has a high content of linoleic acid (omega 6) with a value of 52.68% of the total content of fatty acids in corn oil and 29.70% of oleic acid (omega 9) of the total content of fatty acids in corn oil. The sample presented a value of 12.57% of palmitic acid.Conclusions: Corn oil shows a good content of fatty acids omega 6 and 9. The higher value was of omega 6 with 52.68% content. Corn oil has a good proportion of polyunsaturated of lipids (53.80%) and 14.86% of saturated lipids.

scholarly journals Dietary fish oil modulates macrophage fatty acids and decreases arthritis susceptibility in mice.

1985 ◽  
Vol 162 (4) ◽  
pp. 1336-1349 ◽  
Author(s):  
C A Leslie ◽  
W A Gonnerman ◽  
M D Ullman ◽  
K C Hayes ◽  
C Franzblau ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Fish Oil ◽  
Corn Oil ◽  
Type Ii Collagen ◽  
Chow Diet ◽  
Standard Diet ◽  
Type Ii ◽  
Fish Oil Diet

B10.RIII and B10.G mice were transferred from a diet of laboratory rodent chow to a standard diet in which all the fat (5% by weight) was supplied as either fish oil (17% eicosapentaenoic acid [EPA], 12% docosahexaenoic acid [DHA], 0% arachidonic acid [AA], and 2% linoleic acid) or corn oil (0% EPA, 0% DHA, 0% AA, and 65% linoleic acid). The fatty acid composition of the macrophage phospholipids from mice on the chow diet was similar to that of mice on a corn oil diet. Mice fed the fish oil diet for only 1 wk showed substantial increases in macrophage phospholipid levels of the omega-3 fatty acids (of total fatty acid 4% was EPA, 10% docosapentaenoic acid [DPA], and 10% DHA), and decreases in omega-6 fatty acids (12% was AA, 2% docosatetraenoic acid [DTA], and 4% linoleic acid) compared to corn oil-fed mice (0% EPA, 0% DPA, 6% DHA, 20% AA, 9% DTA, and 8% linoleic acid). After 5 wk this difference between the fish oil-fed and corn oil-fed mice was even more pronounced. Further small changes occurred at 5-9 wk. We studied the prostaglandin (PG) and thromboxane (TX) profile of macrophages prepared from mice fed the two diets just before being immunized with collagen. Irrespective of diet, macrophages prepared from female mice and incubated for 24 h had significantly more PG and TX in the medium than similarly prepared macrophages from male mice. The increased percentage of EPA and decreased percentage of AA in the phospholipids of the macrophages prepared from the fish oil-fed mice was reflected in a reduction in the amount of PGE2 and PGI2 in the medium relative to identically incubated macrophages prepared from corn oil-fed mice. When this same fish oil diet was fed to B10.RIII mice for 26 d before immunization with type II collagen, the time of onset of arthritis was increased, and the incidence and severity of arthritis was reduced compared to arthritis induced in corn oil-fed mice. The females, especially those on the fish oil diet, tended to have less arthritis than the males. These alterations in the fatty acid pool available for PG and leukotriene synthesis suggest a pivotal role for the macrophage and PG in the immune and/or inflammatory response to type II collagen.

Peripheral oxytocin activates vagal afferent neurons to suppress feeding in normal and leptin-resistant mice: a route for ameliorating hyperphagia and obesity

2015 ◽  
Vol 308 (5) ◽  
pp. R360-R369 ◽  
Author(s):  
Yusaku Iwasaki ◽  
Yuko Maejima ◽  
Shigetomo Suyama ◽  
Masashi Yoshida ◽  
Takeshi Arai ◽  
...  
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Body Weight Gain ◽  
Vagal Afferents ◽  
Afferent Neuron ◽  
Afferent Neurons ◽  
Vagal Afferent ◽  
Fos Expression ◽  
Novel Target ◽  
Anorexigenic Effect

Oxytocin (Oxt), a neuropeptide produced in the hypothalamus, is implicated in regulation of feeding. Recent studies have shown that peripheral administration of Oxt suppresses feeding and, when infused subchronically, ameliorates hyperphagic obesity. However, the route through which peripheral Oxt informs the brain is obscure. This study aimed to explore whether vagal afferents mediate the sensing and anorexigenic effect of peripherally injected Oxt in mice. Intraperitoneal Oxt injection suppressed food intake and increased c-Fos expression in nucleus tractus solitarius to which vagal afferents project. The Oxt-induced feeding suppression and c-Fos expression in nucleus tractus solitarius were blunted in mice whose vagal afferent nerves were blocked by subdiaphragmatic vagotomy or capsaicin treatment. Oxt induced membrane depolarization and increases in cytosolic Ca2+ concentration ([Ca2+]i) in single vagal afferent neurons. The Oxt-induced [Ca2+]i increases were markedly suppressed by Oxt receptor antagonist. These Oxt-responsive neurons also responded to cholecystokinin-8 and contained cocaine- and amphetamine-regulated transcript. In obese diabetic db/db mice, leptin failed to increase, but Oxt increased [Ca2+]i in vagal afferent neurons, and single or subchronic infusion of Oxt decreased food intake and body weight gain. These results demonstrate that peripheral Oxt injection suppresses food intake by activating vagal afferent neurons and thereby ameliorates obesity in leptin-resistant db/db mice. The peripheral Oxt-regulated vagal afferent neuron provides a novel target for treating hyperphagia and obesity.

scholarly journals Dietary fat sensing via fatty acid oxidation in enterocytes: possible role in the control of eating

2011 ◽  
Vol 300 (3) ◽  
pp. R554-R565 ◽  
Author(s):  
Wolfgang Langhans ◽  
Claudia Leitner ◽  
Myrtha Arnold
Keyword(s):  
Fatty Acids ◽  
Small Intestine ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Energy Homeostasis ◽  
Vagal Afferents ◽  
Acid Oxidation ◽  
Physiological Relevance ◽  
Vagal Afferent ◽  
Afferent Signaling

Various mechanisms detect the presence of dietary triacylglycerols (TAG) in the digestive tract and link TAG ingestion to the regulation of energy homeostasis. We here propose a novel sensing mechanism with the potential to encode dietary TAG-derived energy by translating enterocyte fatty acid oxidation (FAO) into vagal afferent signals controlling eating. Peripheral FAO has long been implicated in the control of eating ( 141 ). The prevailing view was that mercaptoacetate (MA) and other FAO inhibitors stimulate eating by modulating vagal afferent signaling from the liver. This concept has been challenged because hepatic parenchymal vagal afferent innervation is scarce and because experimentally induced changes in hepatic FAO often fail to affect eating. Nevertheless, intraperitoneally administered MA acts in the abdomen to stimulate eating because this effect was blocked by subdiaphragmatic vagal deafferentation ( 21 ), a surgical technique that eliminates all vagal afferents from the upper gut. These and other data support a role of the small intestine rather than the liver as a FAO sensor that can influence eating. After intrajejunal infusions, MA also stimulated eating in rats through vagal afferent signaling, and after infusion into the superior mesenteric artery, MA increased the activity of celiac vagal afferent fibers originating in the proximal small intestine. Also, pharmacological interference with TAG synthesis targeting the small intestine induced a metabolic profile indicative of increased FAO and inhibited eating in rats on a high-fat diet but not on chow. Finally, cell culture studies indicate that enterocytes oxidize fatty acids, which can be modified pharmacologically. Thus enterocytes may sense dietary TAG-derived fatty acids via FAO and influence eating through changes in intestinal vagal afferent activity. Further studies are necessary to identify the link between enterocyte FAO and vagal afferents and to examine the specificity and potential physiological relevance of such a mechanism.

A high-fat diet attenuates the central response to within-meal satiation signals and modifies the receptor expression of vagal afferents in mice

2009 ◽  
Vol 296 (6) ◽  
pp. R1681-R1686 ◽  
Author(s):  
Wahiba Nefti ◽  
Catherine Chaumontet ◽  
Gilles Fromentin ◽  
Daniel Tomé ◽  
Nicolas Darcel
Keyword(s):  
Food Intake ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
Receptor Expression ◽  
Vagal Afferents ◽  
Afferent Neuron ◽  
Short Term ◽  
Vagal Afferent ◽  
The Brain ◽  
Term Response

During digestion, macronutrients are sensed within the small intestine. This sensory process is dependent upon the action of gut mediators, such as cholecystokinin (CCK) or serotonin (5-HT), on vagal afferents that, in turn, convey peripheral information to the brain to influence the control of food intake. Recent studies have suggested that dietary conditions alter vagal sensitivity to CCK and 5-HT. This phenomenon may be of importance to the onset of eating disorders. The aim of the present study was thus to investigate the effects of subjecting mice to 15 days of either an HF diet (30% fat, 54% carbohydrate) or an NF diet (10% fat, 74% carbohydrate) on 1) daily and short-term food intake, 2) vagal sensitivity to peripheral anorectic factors and macronutrient loads, and 3) vagal afferent neuron receptor expression. The results indicated that compared with an NF diet, and while increasing food intake and body weight gain, an HF diet altered the short-term response to CCK-8 and intragastric macronutrient loads, while decreasing vagal activation by CCK-8 and modifying the receptor expression of vagal neurons. These findings, therefore, suggest that dietary intervention effect on food intake could be linked to changes in vagal afferent receptor profiles.

scholarly journals Hypertonic saline stimulates vagal afferents that respond to lung deflation

2019 ◽  
Vol 317 (6) ◽  
pp. R814-R817
Author(s):  
Juan Guardiola ◽  
Mohamed Saad ◽  
Jerry Yu
Keyword(s):  
Hypertonic Saline ◽  
Single Unit ◽  
Direct Injection ◽  
Control Level ◽  
Receptive Fields ◽  
Vagal Afferents ◽  
Lung Inflation ◽  
Mechanically Ventilated ◽  
Lung Deflation ◽  
Increased Activity

In our present studies, we seek to determine whether increased osmolarity stimulates deflation-activated receptors (DARs). In anesthetized, open-chest, and mechanically ventilated rabbits, we recorded single-unit activities from typical slowly adapting receptors (SARs; responding only to lung inflation) and DAR-containing SARs (DAR-SARs; responding to both lung inflation and deflation) and identified their receptive fields in the lung. We examined responses of these two groups of pulmonary sensory units to direct injection of hypertonic saline (8.1% sodium chloride; 9-fold in tonicity) into the receptive fields. Hypertonic saline decreased the activity in most SAR units from 40.3 ± 5.4 to 34.8 ± 4.7 imp/s ( P < 0.05, n = 12). In contrast, it increased the activity in DAR-SAR units quickly and significantly from 15.9 ± 2.2 to 43.4 ± 10.0 imp/s ( P < 0.01, n = 10). Many units initially had increased activity, mainly in the deflation phase. DAR-SAR activities largely returned to the control level 30 s after injection. Since hypertonic saline stimulated DAR-SAR units but not SAR units, we conclude that hypertonic saline activates DARs.

THE INFLUENCE OF DIETARY FAT ON THE FATTY ACID COMPOSITION OF LIVER, CARCASS, AND MILK OF RATS

1961 ◽  
Vol 39 (12) ◽  
pp. 1855-1863 ◽  
Author(s):  
Joyce L. Beare
Keyword(s):  
Fatty Acids ◽  
Fatty Acid Composition ◽  
Liquid Chromatography ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Dietary Fat ◽  
Rapeseed Oil ◽  
Corn Oil ◽  
Gas Liquid Chromatography ◽  
Long Chain

Fatty acids of liver, carcass, and milk of rats fed corn oil, rapeseed oil, partially hydrogenated herring oil, or margarine were examined by gas–liquid chromatography. Appreciable quantities of linoleic acid were maintained in the tissues and milk, even when the hydrogenated herring oil with a low level of linoleic acid was fed. The proportion of C20and C22acids deposited or secreted was related to that of the diet, and was highest with rapeseed oil. In the livers of rats fed each diet, long-chain, polyunsaturated acids were observed. The fatty acids of milk more closely reflected the dietary pattern than did those of the tissues.

Gastric loads and cholecystokinin synergistically stimulate rat gastric vagal afferents

1993 ◽  
Vol 265 (4) ◽  
pp. R872-R876 ◽  
Author(s):  
G. J. Schwartz ◽  
P. R. McHugh ◽  
T. H. Moran
Keyword(s):  
Food Intake ◽  
Vagal Afferents ◽  
Sufficient Information ◽  
Afferent Activity ◽  
Combined Load ◽  
Synergistic Inhibition ◽  
Afferent Fibers ◽  
Inhibit Food Intake ◽  
Vagal Afferent ◽  
Afferent Response

Both gastric preloads and exogenous cholecystokinin (CCK) administration inhibit food intake, and combinations of preloads and CCK suppress feeding to a greater degree than either stimulus delivered alone. A role for the vagus nerve in mediating CCK's inhibition of food intake has been proposed, and gastric vagal afferent fibers respond to both gastric loads and local CCK infusions. To examine whether combined load and CCK stimuli may synergistically augment gastric neural afferent activity at the level of the peripheral vagus, we have examined the gastric vagal afferent responses (n = 8) to a range of gastric saline loads (1, 2, and 3 ml) and exogenous close celiac arterial CCK (10 and 100 pmol) when administered alone or in combination. Gastric loads ineffective in eliciting a significant increase in vagal afferent activity when administered alone became effective when combined with doses of CCK that were subthreshold for the production of a vagal afferent response. Gastric loads that alone were effective in producing a significant vagal afferent response yielded an even greater response when administered in combination with both subthreshold and suprathreshold doses of CCK. These data demonstrate that, in rats, signals produced by combined gastric load and exogenous CCK administration are integrated peripherally and interact synergistically. These results suggest that signals arising from the vagus may provide sufficient information for the synergistic inhibition of food intake produced by combinations of gastric loads and exogenous CCK.

Dietary lipids and fatty acid deposition in various calf tissues

1963 ◽  
Vol 205 (6) ◽  
pp. 1151-1153 ◽  
Author(s):  
E. S. Erwin ◽  
W. Sterner
Keyword(s):  
Fatty Acids ◽  
Nervous System ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Acid Composition ◽  
Corn Oil ◽  
Dietary Lipids ◽  
Dietary Fatty Acids ◽  
Methyl Myristate

Calves were fed from 5 to 85 days of age a synthetic milk that contained either 10% corn oil (ca. 50% linoleic acid) or 10% methyl myristate. The fatty acid composition of almost all tissues studied was altered to some extent by the change in dietary fatty acids. In the central nervous system, the medulla and spinal cord were resistant, but the peripheral nervous system (sympathetic trunk, brachial plexus, and vagus nerve) profoundly reflected alteration in dietary fatty acids. In peripheral nervous tissue from calves fed corn oil the proportion of linoleic acid increased from 2 to 5% to 25 to 30%. Similarly, in such tissues, myristic acid increased from 2 to 6% to 16 to 43% in methyl myristate-fed calves. Even the fatty acid composition of endocrine glands (pituitary, adrenal, and testis) reflected dietary fatty acids. The fatty acid composition of the skeletal muscle, adipose tissue, and aorta changed with different dietary fats. The greatest change occurred in the cardiac muscle and liver, in which the proportion of linoleic acid increased in the corn oil-fed calves to 50% of the total fatty acids.

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