Seasonal variations of physiological responses, milk production, and fatty acid profile of local crossbred cows in Tunisia.

The study investigates the seasonal variations of physiological responses, milk yield, milk composition, and milk fatty acid profile of local crossbred cows (Friesian × Brown Atlas) in northwestern Tunisia. A total of 80 multiparous cows from smallholder farmers were sampled between 2018 and 2019. The cows were feed the same diet ad libitum and exposed to the same Mediterranean climatic conditions. Weekly rectal temperature (RT; °C), respiratory rate (RR; rpm), and heart rate (HR; bpm) were measured per cow in each season. Individual milk yield and samples were recorded bi-weekly and collected in duplicate for chemical analyses. Milk fatty acids (FAs) were analyzed using gas chromatography-mass spectrometry (GC-MS). Results showed an increase (P < 0.05) in RT (+ 1.3%), RR (+ 12.1%), and HR (+ 9.9%) when the temperature-humidity index (THI) increased from winter (53.6) to summer (74.4) in response to heat stress. Milk yield did not vary significantly between seasons (8.3 L/day on average). Summer milk contained more fat (+ 7.8%) and log SCC (+ 13.7%). The proportion of the monounsaturated (31.2 vs. 27.2%) and polyunsaturated (4.29 vs. 3.86%) FAs decreased (P < 0.05) between winter and summer. Saturated FAs (64.5 vs. 67.7%) were higher (P < 0.05) in summer than in winter. Winter milk fat contained higher levels of C18:2cis-9 trans-11 (CLA) (0.73 vs. 0.56%) and ω-3 FA (0.83 vs. 0.63%), but a lower ω-6/ω-3 ratio (4.07 vs. 6.17%) compared to summer. As the cows were fed the same diet throughout the two seasons, the performances obtained were mainly due to the resistance of the local crossbred cow to the hot conditions. It is concluded that the local crossbred cow maintains its productivity and tolerate the hot Mediterranean climate.

Neural mechanism of the antisecretory effect of peptide YY in the rat colon in vivo.

The purpose of this work was to determine the mechanism of the antisecretory effect of peptide YY in the rat colon and whether this effect is physiological. In this prospect, doses of exogenous peptide YY producing physiological and supraphysiological plasma levels were intravenously infused in rats provided with colonic and jejunal ligated loops in vivo, under secretory stimulation by vasoactive intestinal peptide. Peptide YY decreased the secretory effect of VIP in a dose-related fashion. The effect of peptide YY was blocked or strongly decreased by tetrodotoxin, hexamethonium, idazoxan, haloperidol, and the sigma antagonist BMY 14, 802 in both the colon and jejunum. We conclude that peptide YY decreases water and electrolyte secretion in the colonic mucosa by a complex neural mechanism involving at least two neurons connected through a nicotinic synapse, alpha-2 adrenoceptors and sigma receptors, and that this effect can occur with physiological doses of peptide YY.

Antisecretory effect of peptide YY through neural receptors in the rat jejunum in vitro.

Basal short circuit current (Isc) was measured in stripped rat jejunum after addition of neural antagonists and of peptide YY (PYY). Basal Isc was slightly (by 10-21%) but significantly inhibited by tetrodotoxin, hexamethonium, idazoxan, and the sigma antagonist BMY 14,802. PYY (10(-7) M) reduced basal Isc by approximately 54%. This inhibition was unchanged by hexamethonium but reduced by 44-68% in the presence of tetrodotoxin, idazoxan, haloperidol, BMY 14,802, and atropine. The Y2 agonist pYY(3-36) was more potent than the Y1 agonist (Leu31,Pro34)PYY. In conclusion, PYY reduces basal Isc in rat jejunum in part through a neural mechanism involving muscarinic receptors, alpha2 adrenoceptors, and sigma receptors and, in part, through a direct effect on enterocytes. The PYY effect seems mainly carried out through Y2-receptor activation.

Inhibitory effects of peptide YY on basal and VIP-stimulated short-circuit current in the rat jejunum: influence of technical conditions on observed results.

The interaction of PYY and VIP was studied in stripped and intact rat jejunum preparations mounted in Ussing chambers. PYY decreased basal Isc in intact as well as in stripped jejunum. Stripping was necessary to evidence a stimulation of basal Isc by VIP. When PYY and VIP were administered at the same time in the serosal bath, their effects seemed additive; VIP stimulation took over when VIP was present in ten times larger amounts than PYY, while PYY inhibition predominated at isomolar concentrations (10(-7) M) of both peptides. However, when PYY was administered three to six minutes before isomolar amounts of VIP, the VIP stimulation developed without being notably hampered. At this time, however, the amount of radioimmunoassayable PYY in the serosal compartment represented still 60% of the added amount. In conclusion, the experimental conditions can significantly change the results: stripping the longitudinal muscle/myenteric plexus impairs the effect of PYY and VIP in a different fashion, while the timing and order of administration of the peptides may change the apparent interaction between VIP stimulation and PYY inhibition.

Neural modulation of the antisecretory effect of peptide YY in the rat jejunum.

The endocrine and neural peptide, peptide YY, inhibits intestinal secretion of water and electrolytes in several animal species and in man. Peptide YY receptors have been evidenced on isolated rat jejunal crypt cells, but neural receptors are also likely to participate in the antisecretory effect of peptide YY in vivo. The aim of the present study was to investigate the mechanisms of the peptide YY effect on vasoactive intestinal peptide (VIP)-stimulated jejunal net water flux in the rat. Antagonist experiments using several drugs affecting neurally mediated processes were done for the purpose. A small peptide YY dose (10 pmol/kg) inhibited significantly (P < 0.005) the jejunal net water flux produced by 30 microg/kg per h of VIP. The inhibitory effect of peptide YY was suppressed, or strongly and significantly reduced, by tetrodotoxin, hexamethonium, lidocaine, idazoxan and BMY14,802 (51-(4-fluorophenyl)-4-(-4-(5-fluoro-2pyrimidinyl)-1-piperazinyl)- 1-butanol), whereas devazepide and L-NAME (L-omega-N-arginine methyl ester) had no effect. These results suggest that peptide YY inhibits VIP-stimulated jejunal net water flux in vivo through a neural mechanism implicating the participation of nicotinic synapses, alpha2-adrenoceptors and sigma receptors.

Several receptors mediate the antisecretory effect of peptide YY, neuropeptide Y, and pancreatic polypeptide on VIP-induced fluid secretion in the rat jejunum in vivo.

Several Y receptor subtypes have been cloned and/or pharmacologically characterized that mediate the effects of the regulatory peptides peptide YY (PYY), neuropeptide Y (NPY), and pancreatic polypeptide (PP). These peptides possess antisecretory properties on the intestine. This effect can be blocked in vivo by neural antagonists, suggesting the intervention of neural receptors, although epithelial PYY-preferring receptors have been evidenced on jejunal crypt cells. The purpose of the present experiments was to compare the antisecretory properties in vivo of a series of PYY and NPY derivatives with various affinities for different Y receptor subtypes, in order to determine which subtypes were involved. A model of VIP-stimulated secretion by rat jejunal loops was used. The results were compared with the binding affinities for PYY-preferring receptors determined on rat jejunal crypt cell membranes. Full-length PYY(1-36) was about three times more potent than NPY(1-36), and 10 times more potent than PP in the low dose range. PP, however, had a low efficacy limited to about 50% inhibition of VIP effect. Both Y1 agonists ([Leu31, Pro34]PYY and [Leu31,Pro34]NPY), and Y2 agonists [C-terminal fragments ranging from PYY (3-36) and NPY(3-36) to PYY(22-36) to NPY(22-36)] displayed potent antisecretory properties. PYY derivatives and fragments were always more potent than their respective NPY counterparts. In contrast, Y1 derivatives and PP had very low affinity for the epithelial PYY receptor as measured in vitro by radioreceptor assay. These data suggest that the antisecretory effect of PYY/NPY/PP peptides in vivo involves the effects of several receptors: a Y2-like, PYY-preferring receptor identical to the epithelial receptor, a Y1-like receptor, and a third receptor with high affinity for PP.

[Antisecretory effects of YY peptide and neuropeptide Y at three levels of the small intestine in rats]. / Effets antisécrétoires du peptide YY et du neuropeptide Y à trois niveaux de l'intestin grêle chez le rat.

OBJECTIVES AND METHODS: The purpose of this study was to compare the effects of peptide YY (PYY) and neuropeptide Y (NPY) on VIP- and PGE2-stimulated intestinal net water flux at three different levels of the small intestine (duodenum, jejunum, ileum), by a technique of in situ closed loops in anaesthetised rats. RESULTS: VIP-stimulated net water flux was efficiently inhibited by both peptides at all three intestinal levels studied; PYY (ID50 about 30 pmol/kg.h) was 3 to 18 fold more potent than NPY. PGE2-stimulated net water flux was also efficiently inhibited in the jejunum and ileum; PYY (ID50 about 10 pmol/kg.h) was 30 to 90 fold more potent than NPY. A 30% inhibition of PGE2-stimulated net water flux could only be achieved in the duodenum with the largest dose of either peptide used in this study. CONCLUSIONS: PYY and NPY display potent inhibitory effects of stimulated net water flux at the three studied levels of the small intestine, except in the PGE2-stimulated duodenum. The PYY ID50s measured suggest that PYY may have a physiological action in regulating small intestinal water flux in the rat.

Sequence of rat lipoprotein lipase-encoding cDNA.

A rat lipoprotein lipase (LPL)-encoding cDNA (LPL) has been entirely sequenced and compared to the sequences of all the LPL cDNAs reported in other species. As expected, high homology was found between the coding exons. The putative catalytic triad, Ser132, Asp156, His241, according to human numbering, is conserved in rat. As is the case in mouse, an Asn444 present in human LPL is also missing. The major divergences between human, mouse and rat LPLs were observed in the untranslated exon 10, where (i) the rat cDNA exhibits a 157-bp insertion and an 81-bp deletion relative to human; (ii) neither the B1 repeat nor the homopurine stretch reported in mouse can be recognized, and (iii) the rat cDNA displays several A+T-rich stretches.