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Short chain fatty acid absorption from the human distal colon: interactions between acetate, propionate and calcium.

OBJECTIVE: Our purpose was to conduct a preliminary study to see if propionate and calcium affected acetate absorption, and acetate and calcium affected propionate absorption from the human distal colon. METHODOLOGY: We studied six healthy subjects on eight occasions in randomized order after overnight fasts. Test solutions (300 ml) were infused into the rectum, retained for 30 minutes, and then the infusion fluid was collected for analysis. The infusion solutions contained combinations of sodium acetate (56.25 mmol/L), sodium propionate (18.75 mmol/L) and calcium chloride (50 mmol/L) plus polyethylene glycol (PEG) as an unabsorbable marker. RESULTS: The reduction in the acetate:PEG concentration ratio over 30 minutes after acetate alone, 4.1 +/- 4.2, was significantly less than after acetate plus propionate, 40.2 +/- 11.9, and acetate plus calcium, 34.0 +/- 8.9 (p < 0.05). However, the change in acetate:PEG ratio when acetate, propionate and calcium were all infused together, 13.2 +/- 4.6, was no different from acetate alone. The reduction in the propionate:PEG concentration ratio after propionate alone was 15.7 +/- 3.3, and this was not significantly affected by adding acetate and calcium either alone or together. CONCLUSIONS: We conclude that the absorption of acetate in the rectum and distal colon of humans may be influenced by the presence of calcium and propionate. More detailed kinetic studies are required to confirm these results and characterize the transport mechanisms involved.

Acetates↗

L-Rhamnose increases serum propionate after long-term supplementation, but lactulose does not raise serum acetate.

BACKGROUND: Acute ingestion of the unabsorbed sugar l-rhamnose in humans raises serum propionate, whereas acute ingestion of lactulose raises serum acetate. It is not known whether short-chain fatty acid concentrations in urine and feces reflect those in blood. OBJECTIVE: The objective was to test the effects of oral l-rhamnose and lactulose for 28 d on acetate and propionate concentrations in serum, urine, and feces. DESIGN: Eleven subjects ingested 25 g l-rhamnose, lactulose, or d-glucose (control) for 28 d in a partially randomized crossover design. One fecal sample, hourly blood samples, and all urine samples were collected over 12 h on the last day of each phase. RESULTS: The increase in serum propionate was greater after l-rhamnose than after lactulose (P < 0.05). The effect of lactulose on serum acetate was not significant, but lactulose raised the acetate:propionate ratio compared with d-glucose or l-rhamnose in serum (P < 0.005) and urine (P < 0.02). Flatulence was significantly greater after lactulose and l-rhamnose than after d-glucose (P < 0.0001), an effect that lasted 4 wk with lactulose but only 1 wk with l-rhamnose. CONCLUSIONS: This study confirmed that l-rhamnose ingestion over 28 d continues to selectively raise serum propionate in humans. Although serum acetate did not increase significantly after lactulose, the serum acetate:propionate ratio was significantly different after l-rhamnose and lactulose, which suggests that these substrates could be used to examine the role of colonic acetate and propionate production in the effect of dietary fiber on lipid metabolism. Changes in the ratio of urinary acetate to propionate reflected those in serum.

Acetates↗

Rumen propionate and blood glucose kinetics in growing cattle fed isoenergetic diets.

The relationship between rumen propionate production and blood glucose kinetics was examined in four rumen-fistulated Holstein steers fed isoenergetic amounts of 80/20 (G) and 30/70 (R) grain/chopped alfalfa hay diets at 2-hour intervals. Single-injection rumen propionate and blood glucose kinetics were determined in consecutive 4-hour periods by using [6-3H]glucose intravenously then [1-14C]propionate intraruminally. Rumen propionate specific activity was determined after isolation and quantitation by high-pressure liquid chromatography. Average rumen propionate production rates and pool sizes were 441 g/day and 32.0 g when diet R was fed but increased to 510 g/day (P less than 0.05) and 36.5 g (P less than 0.10), respectively, when diet G was fed. Propionate production as related to digestible energy (DE) intake, averaged 0.56 mole/Mcal DE for R and 0.64 mole/Mcal DE for G. Rumen propionate turnover times were similar for both diets. Despite differences in propionate availability, there were no significant dietary differences in glucose kinetic parameters. Average glucose pool sizes and irreversible losses were 27.0 g and 585 g/day for R and 27.0 g and 582 g/day for G.

Animals↗

Interaction of carnitine and propionate with pyruvate oxidation by hepatocytes from clofibrate-treated rats: importance of coenzyme A availability.

Propionate interferes with normal hepatic metabolic regulation secondary to accumulation of propionyl- and methylmalonyl-CoA. Clofibrate-treatment increases hepatic CoA content and carnitine acetyltransferase activity, both of which may modulate propionate toxicity. Therefore, inhibition of pyruvate oxidation by propionate was studied in hepatocytes isolated from rats maintained on a control or 0.5% clofibrate diet for 7-9 d. Propionate (10 mmol/L) inhibited 14CO2 formation from [1-14C]pyruvate (10 mmol/L) by 60 +/- 2% in hepatocytes from control rats, but by only 46 +/- 3% in cells from clofibrate-treated rats (P less than 0.05). The smaller inhibitory effect of propionate in hepatocytes from clofibrate-treated rats occurred despite increased cellular propionyl-CoA content as compared with controls, but was associated with increased CoASH and total CoA contents. Despite greater carnitine acetyltransferase activity (20-fold) and propionylcarnitine production (2.5-fold) in hepatocytes from clofibrate-treated rats, reversal of propionate's inhibition of pyruvate oxidation by 10 mmol/L carnitine was small (8.7 +/- 3.9%) and not different from that observed in cells from control animals (6.7 +/- 2.4%). Carnitine (10 mmol/L) decreased hepatocyte total acid-soluble CoA content by 20-30% in cells from both control and clofibrate-treated rats. This carnitine-induced decrease in CoA content may limit the efficacy of carnitine under conditions of acyl-CoA accumulation. Clofibrate-induced increased CoA content provides partial protection against propionate toxicity. Metabolic toxicity of propionate is the result of both the increased cellular propionyl-CoA content and the depletion of cellular unesterified CoA.

Animals↗

Role of dietary propionic acid and bile acid excretion in the hypocholesterolemic effects of oligosaccharides in rats.

The aim of this study was to evaluate the influence of dietary propionic acid and bile acid excretion on the hypocholesterolemic effect of fibers. For this purpose, rats were adapted to a diet containing 10 g inulin, 10 g beta-cyclodextrin, or 2.5 g calcium propionate per 100 g diet. Both the inulin and beta-cyclodextrin diets elicited high propionic acid fermentations in the cecum (approximately 45% of total short-chain fatty acids) with relatively low molar proportions of acetic and butyric acids. In rats fed the three experimental diets, 5-7 mumol/min of propionic acid was absorbed in the portal vein, and propionic acid was entirely metabolized by the liver. Plasma cholesterol was more effectively depressed by the beta-cyclodextrin diet than by the inulin diet; the propionic acid-supplemented diet was ineffective in this respect. The inulin diet slightly increased fecal bile acid excretion, compared with the control diet, whereas beta-cyclodextrin markedly enhanced (1.8-fold) bile acid excretion. Microsomal hydroxymethylglutaryl-CoA (HMG-CoA) reductase activity was slightly depressed in rats fed the propionic acid-supplemented diet, whereas it was enhanced by the beta-cyclodextrin diet in parallel to the activity of cholesterol 7 alpha-hydroxylase. The present data suggest that absorption and further hepatic metabolism of large amounts of propionic acid are not sufficient to counteract the induction of HMG-CoA reductase resulting from bile acid fecal losses. The rise of these losses plays a major role in the hypocholesterolemic effect of beta-cyclodextrin.

Absorption↗

Effects of high zinc diets using zinc propionate on molt induction, organs, and postmolt egg production and quality in laying hens.

This study was conducted to determine the ability of an alternative salt form of 1% Zn, Zn propionate, to induce molt in 66-wk-old hens. The hens were randomly assigned to 4 treatment groups of 27 or 28 birds each: a) molted conventionally by feed withdrawal, b) 1% Zn as Zn acetate, c) 1% Zn as Zn propionate, or d) nonmolted control for 9 d. Feed intake was (P < 0.05) depressed in Zn acetate and Zn propionate hens when compared with nonmolted control hens during the 9 d. Ovary weights of hens undergoing feed withdrawal, Zn acetate, or Zn propionate were not (P > 0.05) different from each other, but all were (P < 0.05) lighter than the ovary weights of nonmolted control hens. Zinc concentrations in the kidney and liver were (P < 0.05) increased in Zn acetate and Zn propionate molted hens when compared with nonmolted hens on the control diet or hens molted by feed withdrawal. Bone ash values were (P < 0.05) increased for Zn acetate and Zn propionate molted hens or nonmolted control hens as compared with molted hens on feed withdrawal. Over the entire 3-mo postmolt period, there were no significant differences in interior egg qualities, but egg weights from hens fed Zn propionate were (P < 0.05) heavier than those from hens on feed withdrawal. The data of the current study demonstrated that feeding a Zn propionate (1% zinc)-supplemented diet can induce molt.

Animal Feed↗

Neural and non-neural mediation of propionate-induced contractile responses in the rat distal colon.

Short-chain fatty acids (SCFAs), including propionate, butyrate and acetate, are fermentation products of carbohydrates in the colon. We investigated the contractile effects of SCFAs on the rat distal colon. Mechanical activity of the circular muscle in strip preparations was recorded in vitro. Propionate and butyrate concentration-dependently (10 micromol L(-1)-10 mmol L(-1)) induced rapid, large amplitude phasic contractions (the first phase) followed by tonic contractions (the second phase). Acetate itself had no effect on muscle activity, although preincubation with acetate attenuated both phases of the propionate-induced response. The propionate-induced phasic contraction was attenuated by atropine, tetrodotoxin and the 5-HT4 receptor antagonist SB-204070. The propionate-induced tonic contraction was attenuated by the cyclo-oxygenase inhibitor piroxicam. Antagonists of 5-HT1A, 5-HT2A and 5-HT3 receptors had no effect on the responses. Propionate-induced responses were not observed in mucosa-free preparations. These results suggest that propionate acts on receptors in the mucosa causing the release of 5-HT from enterochromaffin cells. 5-HT acts through 5-HT4 receptors on the endings of intrinsic primary afferent neurones that in turn activate cholinergic motor neurones that contract the circular muscle. Propionate also causes tonic contraction, via prostaglandin release, in the rat distal colon.

Acetates↗

Effect of propionate toxicity on methanogen-enriched sludge, Methanobrevibacter smithii, and Methanospirillum hungatii at different pH values.

The effect of propionate toxicity at different pH values (6.5, 7.0, and 8.0) on methanogen-enriched sludge. Methanobrevibacter smithii, and Methanospirillum hungatii was studied. Organisms were grown in Balch medium 3 in Hungate tubes, and toxicity was characterized by a decrease in production of methane and in bacterial numbers. Propionate inhibited bacterial growth and cumulative methane production at concentrations as low as 20 mM. In the absence of propionate, the methanogen-enriched sludge and M. smithii showed better cumulative methane production at pH 6.5 and 7.0 than at pH 8.0. However, in the presence of propionate, these organisms showed better cumulative methane production at pH 8.0. M. hungatii differed in its behavior; the best values of cumulative methane production for this organism occurred at pH 7.0. Bacterial numbers reflected the microbial response to the presence of propionate. The highest counts of methanogenic bacteria were observed at pH 6.5 and 8.0. The numbers of methanogens were affected by the presence of propionate even at concentrations as low as 20 or 30 mM; at propionate concentrations above 80 mM, the methanogen count was affected by at least 2 orders of magnitude. Upon comparison of the responses of the pure cultures and the methanogen-enriched sludge to increasing propionate concentrations, it was found that the sensitivity of the pure cultures was similar to that of the methanogens in the sludge.

Colony Count, Microbial↗

Propionate induces polymorphonuclear leukocyte activation and inhibits formylmethionyl-leucyl-phenylalanine-stimulated activation.

Short-chain carboxylic acids (SCCA) are metabolic by-products of bacterial pathogens which can alter cytoplasmic pH and inhibit a variety of polymorphonuclear leukocyte (PMN) motile functions. Since cytoskeletal F-actin alterations are central to PMN mobility, in this study we examined the effects of SCCA on cytoskeletal F-actin. Initially, we tested nine SCCA (formate, acetate, propionate, butyrate, valerate, caproate, lactate, succinate, and isobutyrate). We document here that while eight altered cytoplasmic pH, only six altered cytoskeletal F-actin. We then selected one SCCA that altered both F-actin and cytoplasmic pH (propionate) and one SCCA that altered only cytoplasmic pH (lactate) for further study. Propionate, but not lactate, caused an irregular cell shape and F-actin distribution. Furthermore, propionate, but not lactate, inhibited formylmethionyl-leucyl-phenylalanine (fMLP)-stimulated PMN polarization, F-actin localization, and cytoplasmic pH oscillation. Propionate-induced changes in cytoskeletal F-actin and cytoplasmic acidification were not affected by the fMLP receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine; however, alkalinization was affected. Pertussis toxin treatment completely inhibited propionate-induced changes in F-actin but had no effect on propionate-induced cytoplasmic pH oscillation. These results indicate that propionate (i) bypasses the fMLP receptor and G protein(s) to induce cytoplasmic pH oscillation, (ii) operates through G protein(s) to induce actin oscillation, cell shape changes (to irregular), and F-actin localization, and (iii) inhibits fMLP-stimulated cytoplasmic pH and actin oscillation, PMN polarization, and F-actin localization.

Actins↗

Addition of dimethylsulphoxide to methyl-tert-butyl ether and ethyl propionate increases cholesterol dissolving capacity and cholesterol gall stone dissolution in vitro.

There is a discrepancy between in vitro cholesterol dissolving efficacy of methyl-tert-butyl ether (MTBE) and ethyl propionate and cholesterol gall stone dissolution in vivo. This study investigated whether the presence of bile changes the cholesterol dissolving capacity of MTBE and ethyl propionate. The addition of dimethylsulphoxide to MTBE or ethyl propionate was also studied to discover if it improves the dissolving capacity for cholesterol gall stones. The presence of bile caused a 25% decrease in cholesterol dissolving capacity of both MTBE and ethyl propionate (p < 0.0001). This inhibitory effect of bile could be overcome by the addition of dimethyl-sulphoxide: dimethylsulphoxide caused an increase in cholesterol dissolving capacity of MTBE and ethyl propionate, the increase depending on the dimethyl-sulphoxide/bile ratio in the mixture. Mean dissolution time of weight, size, and patient matched cholesterol gall stones was 220 minutes in MTBE and 130 minutes in MTBE/dimethylsulphoxide (p < 0.0001). No stones dissolved completely in ethyl propionate or ethyl propionate/dimethyl-sulphoxide within 300 minutes. In conclusion, MTBE/dimethylsulphoxide is a more potent dissolving agent for cholesterol gall stones than MTBE, giving a 40% reduction in dissolution time. Addition of dimethylsulphoxide to ethyl propionate does not result in faster stone dissolution. MTBE and MTBE/dimethylsulphoxide are far superior to ethyl propionate as solvents for cholesterol gall stones.

Bile↗

Propionate induces cell swelling and K+ accumulation in shark rectal gland.

Small organic anions have been reported to induce cell solute accumulation and swelling. To investigate the mechanism of swelling, we utilized preparations of rectal gland cells from Squalus acanthias incubated in medium containing propionate. Propionate causes cells to swell by diffusing across membranes in its nonionic form, acidifying cell contents, and activating the Na+-H+ antiporter. The Na+-H+ exchange process tends to correct intracellular pH (pHi), and thus it maintains a favorable gradient for propionic acid diffusion and allows propionate to accumulate. Activation of the Na+-H+ antiport also facilitates Na+ entry into the cell and Nai accumulation. At the same time Na+-K+-ATPase activity, unaffected by propionate, replaces Nai with Ki, whereas the K+ leak rate, decreased by propionate, allows Ki to accumulate. As judged by 86Rb+ efflux, the reduction in K+ leak was not due to propionate-induced cell acidification or reduction in Cli concentration. Despite inducing cell swelling, propionate did not disrupt cell structural elements and F actin distribution along cell membranes.

Actins↗

Effect of short-term propionate infusion on feed intake and blood parameters in sheep.

The hypothesis that propionate is a short-term feed intake-regulating agent was studied. Mature wether sheep were infused over 20 min with Na propionate into the mesenteric vein, while feed intake and feeding pattern were monitored over 1.5 h. Feed intake was reduced by infusions at 2 mmol/min, which were associated with marked increases in jugular as well as portal concentrations of insulin, glucose, and propionate. In a second experiment, animals were infused with 2 mmol/min Na propionate into the portal vein. No decrease in feed intake was observed, although there were similar increases in insulin, glucose, and propionate as found in mesenteric vein-infused animals. It is concluded that mesenteric propionate in high doses acts as a satiety factor. Possible explanations for the difference between site of infusion may be a different distribution of the infusate over the liver and/or the presence of propionate-sensitive receptors in the mesenteric/portal vein region. It seems unlikely that insulin concentrations are involved in inducing satiety in propionate-infused animals.

Animals↗

Anaplerotic effects of propionate on oxidations of acetate and long-chain fatty acids.

Studies were performed to test the influence of propionate as a competing myocardial substrate on acetate and palmitate metabolism in reperfused pig hearts after an exposure of mild-to-moderate regional ischemia. Experiments were conducted in intact, working pig hearts (n = 10) using an extracorporeal coronary perfusion technique. Half the animals received 2 mM propionate selectively into the anterior descending (LAD) perfusate. Perfusion conditions in the LAD circulation were divided into three intervals: an aerobic, preischemic period (0-20 min); an ischemic period affected by a 60% reduction in LAD flow (20-60 min); and an aerobic, postischemic period (60-100 min). Steady-state infusions of (1(-14)C) acetate and [9, 10(-3)H] palmitate were begun at 60 min perfusion to monitor metabolism during reperfusion. Propionate had no effect on oxidation of acetate except for a slight delay in CO2 appearance. Propionate significantly suppressed oxidation of long-chain fatty acids (-38 delta %, P < 0.018), which was not explained by a selective scavenging of CoA units or carnitine by propionate, which might otherwise enhance fatty acid activation, transfer, or oxidation. Propionate by indirect estimates had no apparent effect on glucose metabolism. Propionate-treated hearts, despite shifts in substrate preference, were not further compromised in energy metabolism as levels of creatine phosphate and adenine nucleotides were comparable to control hearts. Recovery of regional mechanical function was also comparable between groups but incompletely, with respect to preischemic performance, compatible with myocardial stunning. The data show in reperfused myocardium that propionate is capable of altering the preferred use of fatty acids, but that anaplerotic entry of carbon units during this reperfusion interval was sufficient to prevent a selective imbalance of energy metabolism or deficit in mechanical recovery.

Acetates↗

Effects of butyrate and propionate on the adhesion, growth, cell cycle kinetics, and protein synthesis of cultured human gingival fibroblasts.

BACKGROUND: Various periodontal and root canal pathogens, such as the Bacteroides species, can produce significant amounts of short chain fatty acids (SCFA). The roles of SCFA in the pathogenesis of periodontal disease are still not fully understood. METHODS: We therefore investigated 2 main SCFA, butyrate and propionate, on the functional behavior of cultured human gingival fibroblasts (GF) such as cell growth, protein synthesis, cell adhesion capacity, and cell cycle progression. RESULTS: Butyrate and propionate inhibited the growth of healthy (HGF) and inflamed gingival fibroblasts (IGF) in a dose dependent manner. At concentrations of 4, 8, and 16 mM, butyrate suppressed the cell growth by 11 to 58%, 16 to 60%, and 50 to 71%, respectively. The response of cultured gingival fibroblasts to SCFA showed individual differences. Morphologically, GF became larger and more flattened in appearance following exposure to butyrate (>8 mM) and propionate (>24 mM) for 5 days. Inhibitory effects of butyrate (>2 mM) and propionate (>8 mM) on the growth of GF were due possibly to their inhibition of cell-cycle progression. At concentrations of 2 and 8 mM, butyrate led to G0/G1 arrest. Elevation of the exposure concentration to 8 to 24 mM further result in G2/M phase arrest of GF. On the other hand, propionate, at concentrations ranging from 4 to 24 mM, led to G0/G1 arrest. Butyrate (>2 mM) inhibited the proline-rich protein synthesis of GF. At concentrations of 4, 8, 16, and 24 mM, butyrate inhibited the protein synthesis of HGF-1 by 42%, 43%, 51%, and 54%, respectively. In all strains of cultured GF, the suppressive effect of propionate is less than that of butyrate. At concentration range of 4 to 24 mM, propionate suppressed the protein synthesis of HGF-1 by 23 to 43%. However, both butyrate and propionate (4 to 48 mM) exerted little effects on the adhesion of GF to type I collagen within 3 hours of incubation. CONCLUSIONS: These results suggested that SCFA released by pathogenic microorganisms can contribute to the gingival tissue dysfunction and breakdown through their actions on specific biological functions of GF.

Butyrates↗

Propionate modulates spontaneous contractions via enteric nerves and prostaglandin release in the rat distal colon.

Short-chain fatty acids, such as propionate and acetate, are produced by a bacterial fermentation of carbohydrates in the colonic lumen. We examined the effects of propionate on the frequency and mean amplitude of spontaneous giant contractions (GCs) in circular muscle strips of the rat distal colon with the mucosa attached. An addition of propionate increased the frequency of GCs for about 20 min (> or =1 mm), but the mean amplitude was decreased (> or =0.1 mm). The propionate-induced increase in the frequency of GCs was blocked by the muscarinic acetylcholine receptor antagonist, atropine. In contrast, the nicotinic receptor antagonist, hexamethonium, augmented the response. The propionate-induced decrease in the mean amplitude of GCs was prevented by the cyclooxygenase inhibitor, piroxicam. A pretreatment of the tissues with acetate prevented the propionate-induced modulations of the frequency and amplitude of GCs. These results suggest that propionate increases the frequency of GCs by an activation of cholinergic motor neurons and decreases the mean amplitude by a prostaglandin release. Propionate as well as acetate may be involved in the regulation of spontaneous circular muscle activity in the rat distal colon.

Acetates↗

Effects of glycine and bovine serum albumin on inhibition of propionate metabolism in ovine hepatocytes caused by reduced phenolic monomers.

Hepatocytes isolated from sheep were incubated in the presence of reduced phenolics and glycine to determine the effects of these compounds on hepatic propionate metabolism in vitro. 3-Phenyl-propionic (PPA) or t-cinnamic (CA) acids, but not benzoic (BA) or 3-(4-hydroxyphenyl)propionic (4OHPPA) acids, decreased conversion of propionate to glucose at .05 mM in the absence of supplemental glycine. At 1.2 mM, all reduced phenolics decreased conversion of propionate to glucose in the absence of supplemental glycine. Addition of glycine to the incubation medium linearly alleviated the inhibition by BA, PPA, or CA, suggesting that physiological glycine concentrations limited alleviation of inhibition of propionate metabolism. Hippuric acid production increased as glycine concentration increased in the presence of PPA, CA, or 4OHPPA. Bovine serum albumin did not alleviate inhibition of conversion of propionate to glucose caused by BA, PPA, or CA and slightly alleviated inhibition caused by 4OHPPA (.4 mM). Of the reduced phenolics tested, PPA is the most likely to inhibit gluconeogenesis from propionate in ovine liver in vivo.

Animals↗

Preference for flavored wheat straw by lambs conditioned with intraruminal infusions of acetate and propionate.

We hypothesized that volatile fatty acids in rumen fluid are feedback signals that can condition food preferences or aversions in sheep. Three predictions were tested based on this hypothesis: 1) low doses of sodium propionate or sodium acetate condition preferences, but high doses condition aversions (Exp. 1 and 2); 2) preferences are not caused by osmotic load (Exp. 3 and 4); and 3) low doses of mixtures of acetate:propionate condition preferences (Exp. 4). In Exp. 1, 2, and 4, lambs were divided into four groups (10 lambs/group), and lambs in Exp. 3 were divided into two groups (five lambs/group). In all experiments, alfalfa pellets were the basal diet. On even days, half of the lambs were offered chopped wheat straw containing a distinctive flavor, whereas the other half received straw with a different flavor. During straw ingestion, different groups of lambs received intraruminal infusions of different concentrations (4, 8, or 12% of the daily DE received) of sodium propionate (Exp. 1), sodium acetate (Exp. 2), NaCl at osmotic loads equivalent to those when propionate supplied 4% of the daily DE received (Exp. 3), or different proportions of sodium acetate:sodium propionate (55:45 or 75:25% of the DE of the infusion [4% of the daily DE received]), or equimolar amounts of NaCl (Exp. 4). On odd days, the flavors were switched, and no infusions were administered. After 8 d of conditioning, lambs were offered a choice of wheat straw with the two distinctive flavors. Lambs preferred the flavor paired with the lowest doses of propionate (P = .07) and acetate (P = .08) but avoided the highest doses (P < .001). Excesses of VFA may condition aversions due to increases in rumen fluid osmolality and(or) excessive rates of supply of energy or sodium to the rumen. Lambs also preferred flavored straw associated with combinations of acetate and propionate (P < .001), especially at the highest concentration of propionate (P = .10). Lambs avoided NaCl in Exp. 3 (P < .001) and did not form preferences for NaCl in Exp. 4 (P > .05). Thus, osmolalities were not responsible for flavor preferences. In conclusion, our results support the hypothesis that food preferences and aversions reside along a continuum that depends on the amount of VFA infused.

Acetates↗

Influence of intrajugular administration of insulin, glucagon and propionate on voluntary feed intake of sheep.

The effect of intrajugular injections of insulin, glucagon and propionate, administered singly and in combination, as possible peripheral feedbacks in the control of feed intake in wethers was studied. A complete mixed diet (25% chopped hay: 75% cracked corn) was fed ad libitum. The treatments were saline, 6 mU insulin/kg body weight (BW), 9 ng glucagon/kg BW and 1.3 mg propionate/kg BW. In Exp. 1, five wethers were given the treatments at the beginning of each spontaneous meal over a 24-hr period, and total daily feed intakes were measured. The average number of injections per sheep for a 24-hr period was eight. In Exp. 2, the effects of the treatments on plasma concentrations of insulin, glucagon, propionate and glucose at 15, 30, 60 and 120 min after injection were measured in six other wethers. In Exp. 1, insulin (P less than .01), glucagon (P less than .01), insulin plus propionate (P less than .05) and glucagon plus propionate (P less than .05) decreased 24-hr feed intake by 18.5, 15.8, 11.0 and 11.8%, respectively, compared to the saline control. In Exp. 2, plasma insulin concentrations were increased (P less than .05) at 15 min after administration of insulin and insulin plus propionate, to 2.0 and 2.1 times the preinjection levels, respectively. Glucagon concentrations in plasma were increased (P less than .01) at 15 min after the injection of glucagon, to 2.0 times the pretreatment values. Insulin and glucagon concentrations in plasma were increased only slightly (P less than .10) after administration of glucagon plus propionate. No treatments affected glucose or propionate concentrations in the plasma. Increases in plasma concentrations of insulin, glucagon and propionate may interact directly or initiate other mechanisms involved in the short-term control of feed intake by sheep on a concentrate diet.

Animals↗