Growth hormone-releasing hormone and somatostatin concentrations in the hypophysial portal blood of conscious sheep during the infusion of growth hormone-releasing peptide-6

The effects of growth hormone-releasing peptide-6 (GHRP-6) on peripheral plasma concentrations of growth hormone (GH) and hypophysial portal plasma concentrations of growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) were investigated in conscious ewes. Paired blood samples were collected from the hypophysial portal vessels and from the jugular vein of nine ewes for at least 2 hr. The sheep were then given a bolus injection of 10 μg of GHRP-6 per kg followed by a 2-hr infusion of GHRP-6 (0.1 μ/kg · hr). Blood sampling continued throughout the infusion and for 2 hr afterwards. An increase in plasma GH concentration was observed in the jugular samples of six of the nine ewes (1.4 ± 0.3 vs 7.4 ± 2.0 ng/ml, P < 0.05) 5–10 min after the GHRP-6 bolus injection, but in no case did we observe a significant coincident release of GHRH. During the infusion period, mean plasma GHRH levels were not significantly increased but there was a 50% increase (P < 0.05) in GHRH pulse frequency; GHRH pulse amplitude was not changed. Mean SRIF concentration, pulse frequency, and pulse amplitude were unchanged by GHRP-6 treatment. These data indicate that GHRP-6 causes a small, but significant effect on the pulsatile secretion of GHRH, indicating action at the hypothalamus or higher centers of the brain. The large initial GH secretory response to GHRP-6 injection does not appear to be the result of GHRP-6 action on GHRH or SRIF secretion.     

Relationships between plasma concentrations of leptin and other metabolic hormones in GH-transgenic sheep infused with glucose

To study the regulation of leptin secretion in sheep, we infused glucose (0.32 g/h/kg for 12 h) into GH-transgenic animals (n = 8) that have chronically high plasma concentrations of ovine GH and insulin, but low body condition and low plasma leptin concentrations, and compared the responses with those in controls (n = 8). In both groups, the infusion increased plasma concentrations of glucose and insulin within 1 h and maintained high levels throughout the infusion period (P < 0.0001). Compared with controls, GH-transgenics had higher concentrations of insulin, IGF-1, GH (all P < 0.0001) and cortisol (P < 0.05), but lower GH pulse frequency (P < 0.0001). Overall, leptin concentrations were lower in GH-transgenics than in controls (P < 0.01). A postprandial increase in leptin concentrations was observed in both groups, independently of glucose treatment, after which the values remained elevated in animals infused with glucose, but returned to basal levels in those infused with saline, independently of transgene status. In both GH-transgenics and controls, glucose infusion did not affect the concentrations of GH, IGF-1, or cortisol. In conclusion, GH-transgenic and control sheep show similar responses to glucose infusion for leptin and other metabolic hormones, despite differences between them in body condition and basal levels of these hormones. Glucose, insulin, GH, IGF-1 and cortisol are probably not major factors in the acute control of leptin secretion in sheep, although sustained high concentrations of GH and IGF-1 might reduce adipose tissue mass or inhibit leptin gene expression.     

Effects of amino acids infused into the vein on ghrelin‐induced GH,insulin and glucagon secretion in lactating cows

To investigate the effects of amino acids on ghrelin‐induced growth hormone (GH), insulin and glucagon secretion in lactating dairy cattle, six Holstein cows were randomly assigned to two infusion treatments in a cross‐over design. Mixture solution of amino acids (AMI) or saline (CON) was continuously infused into the left side jugular vein via catheter for 4 h. At 2 h after the start of infusion, synthetic bovine ghrelin was single injected into the right side jugular vein through the catheter. Ghrelin injection immediately increased plasma GH, glucose and non‐esterified fatty acids (P < 0.05) with no difference between both treatments. Additionally, plasma insulin and glucagon concentrations were increased by ghrelin injection in both treatments. The peak value of plasma insulin concentration was greater in AMI compared with CON (P < 0.05). Plasma glucagon concentration showed no difference in the peak value reached at 5 min between both treatments, and then the plasma levels in AMI compared with CON showed sustained higher values (P < 0.05). After plasma glucose concentration reached the peak, the decline was greater in AMI compared with CON (P < 0.05). These results showed that the increased plasma amino acids may enhance ghrelin action which in turn enhances insulin and glucagon secretions in lactating cows.     

Propionate is not an important regulator of plasma leptin concentration in dairy cattle

Propionate was recently shown to increase leptin synthesis in rodents. To determine if a similar effect occurs in ruminants, propionate was administered to lactating dairy cows. In experiment 1, 31 cows were given an intrajugular Na propionate bolus (1,040 micromol/kg body weight), increasing plasma propionate from 160 to 5,680 microM and plasma insulin from 6.8 to 77.8 microIU/mL. Plasma leptin concentration decreased from 2.11 ng/mL before bolus to 1.99 ng/mL after dosing (P<0.05) with no differences in leptin concentrations at 20, 50, and 100 min post-bolus (P>0.10). In experiment 2, 12 cows were used in a duplicated 6 x 6 Latin square experiment to assess the dose-response effect of ruminal propionate infusion on plasma leptin concentration. Sodium propionate was infused at rates of 0, 260, 520, 780, 1040, or 1,300 mmol/h, while total short-chain fatty acid infusion rate was held constant at 1,300 mmol/h by addition of Na acetate to the infusate. Coccygeal blood was sampled following 18 h of infusion. Increasing the rate of propionate infusion linearly increased plasma propionate concentration from 180 to 330 microM (P<0.001) and plasma insulin concentration from 6.7 to 9.1 microIU/mL (P<0.05). There was a quadratic response in plasma leptin concentration (P=0.04) with a maximum at 780 mmol/h propionate, but leptin concentrations increased by no more than 8% relative to the 0 mmol/h propionate infusion. Leptin concentrations were correlated with insulin concentrations but not with propionate concentrations in plasma. Propionate is not a physiological regulator of leptin secretion in lactating dairy cows.     

The effect of season and monensin sodium on the digestive characteristics of autumn and spring pasture fed to sheep

The effects of season of growth and monensin treatment on ruminal digestion of fresh-cut autumn and spring pasture were measured in a single group of ruminally fistulated castrated male sheep, housed indoors in metabolism crates. Responses were assessed in terms of ruminal volatile fatty acid molar proportions, ammonia concentration, pH, apparent digestibility of the pasture, and nitrogen balance of the animals. Blood plasma concentrations of insulin, glucose, beta-hydroxybutyrate, urea, and NEFA were also evaluated. Autumn pasture contained significantly lower proportions of water-soluble carbohydrate (P < 0.05), cellulose (P < 0.05), and lignin (P < 0.05) and increased pectin (P < 0.05), hemicellulose (P < 0.05), and crude protein (P < 0.10) concentrations when compared with spring pasture. Voluntary DMI by sheep of autumn pasture was lower (P < 0.01) than that of spring pasture and was significantly (P < 0.05) reduced by monensin treatment. Monensin treatment significantly decreased the ruminal molar proportions of acetic acid (P < 0.10) and butyric acid (P < 0.001) and increased the molar proportions of propionic acid (P < 0.001) and minor VFA (P < 0.01). Nitrogen retention of the sheep was significantly (P < 0.05) reduced by monensin treatment. Plasma glucose levels were increased (P < 0.10) by monensin treatment during the fourth 5-d collection period in both seasons. Chemical analysis suggested that the composition of autumn pasture was different from that of spring pasture and that this was manifested in vivo by increased DMI and digestibility of spring vs autumn pasture. Ruminal fermentation of autumn pasture also had an increased acetate-to-propionate ratio compared with spring pasture. Monensin treatment acted consistently across seasons by increasing the proportion of propionate and decreasing the proportion of acetate in ruminal fluid.     

Effects of volatile fatty acid supply on their absorption and on water kinetics in the rumen of sheep sustained by intragastric infusions

Three sheep fitted with a ruminal cannula and an abomasal catheter were used to study water kinetics and absorption of VFA infused continuously into the rumen. The effects of changing VFA concentrations in the rumen by shifting VFA infusion rates were investigated in an experiment with a 3 x 3 Latin square design. On experimental days, the animals received the basal infusion rate of VFA (271 mmol/h) during the first 2 h. Each animal then received VFA at a different rate (135, 394, or 511 mmol/h) for the next 7.5 h. Using soluble markers (polyethylene glycol and Cr-EDTA), ruminal volume, liquid outflow, apparent water absorption, and VFA absorption rates were estimated. There were no significant effects of VFA infusion rate on ruminal volume and water kinetics. As the VFA infusion rate was increased, VFA concentration and osmolality in the rumen were increased and pH was decreased. There was a biphasic response of liquid outflow to changes in the total VFA concentration in the rumen, as both variables increased together up to a total VFA concentration of 80.1 mM, whereas, beyond that concentration, liquid outflow remained stable at an average rate of 407 mL/h. There were significant linear (P = 0.003) and quadratic (P = 0.001) effects of VFA infusion rate on the VFA absorption rate, confirming that VFA absorption in the rumen is mainly a concentration-dependent process. The proportion of total VFA supplied that was absorbed in the rumen was 0.845 (0.822, 0.877, and 0.910 for acetate, propionate, and butyrate, respectively). The molar proportions of acetate, propionate, and butyrate absorbed were affected by the level of VFA infusion in the rumen, indicating that this level affected to a different extent the absorption of the different acids.     

Effects of Ostertagia ostertagi infection on secretion of metabolic hormones in calves.

Effects of Ostertagia ostertagi infection on secretion of insulin, pancreatic glucagon, cortisol, gastrin, and pepsinogen were studied in calves inoculated with 100,000 (group 1) or 10,000 (group 2) O ostertagi infective larvae weekly for 14 weeks. Plasma insulin concentrations in both inoculated groups were lower than those in a non-infected (group 3) control group. The differences between group 1 and group 3 were significant (P < 0.05) at 2 and 12 weeks after initial inoculation. Plasma pancreatic glucagon and cortisol concentrations of groups 1 and 2 did not differ significantly from those of the control group, although plasma pancreatic glucagon concentration was consistently lower in group-1 calves from 4 weeks to end of the study. Plasma pepsinogen and serum gastrin concentrations also increased significantly (P < 0.05) in both groups that received inoculations. We concluded that decreased plasma insulin concentrations are contributory to changes in postabsorptive protein metabolism, and that serum gastrin concentrations are more representative of the pathologic changes in the abomasum than are plasma pepsinogen concentrations.     

Effects of adding valerate, caproate, and heptanoate to ruminal buffers on splanchnic metabolism in steers under washed-rumen conditions

Four steers fitted with a ruminal cannula and chronic indwelling catheters in the mesenteric artery, mesenteric vein, hepatic portal vein, hepatic vein, and the right ruminal vein were used to study VFA absorption from bicarbonate buffers incubated in the washed reticulorumen, and metabolism by splanchnic tissues. Portal and hepatic vein blood flows were determined by infusion of p-aminohippurate into the mesenteric vein. The steers were subjected to four experimental treatments in a Latin square design. The treatments were Control (ruminal bicarbonate buffer with [mmol/kg]: acetate = 72; propionate = 30; isobutyrate = 2.1; butyrate = 12; valerate = 1.2; caproate = 0; and heptanoate = 0); Val (same as control except for valerate = 8 mmol/kg); Cap (same as control except for caproate = 3.5 mmol/kg); and Hep (same as control except for heptanoate = 3 mmol/kg). All buffers were incubated for 90 min in the rumen, and ruminal VFA absorption rates were maintained by continuous intraruminal infusion of VFA. The arterial concentrations of valerate and heptanoate showed a small increase (< or = 1 micromol/L; P < 0.05) with inclusion of the respective acid in the ruminal buffer, but no change (P = 0.57) in arterial concentration of caproate was detected. Valerate increased (P < 0.05) the net portal flux of butyrate and valerate, as well as the net splanchnic flux of propionate, butyrate, and valerate. With Cap and Hep, the net portal flux of caproate and heptanoate accounted for 54 and 45% of ruminal disappearance rates, respectively, indicating that these acids were extensively metabolized by the ruminal epithelium. Caproate was ketogenic both in the ruminal epithelium and in the liver, and Cap increased (P < 0.05) the arterial concentration, ruminal vein minus arterial concentration difference, net hepatic flux, and net splanchnic flux of 3-hydroxybutyrate. The net hepatic flux of glucose decreased (P = 0.02) with Cap and Hep compared with Control and Val; however, no effect (P = 0.14) on the net splanchnic flux of glucose could be detected. We conclude that the strong biological activity of valerate, caproate, and heptanoate warrant increased emphasis on monitoring their ruminal presence and their potential systemic effects on ruminant metabolism.     

Impact of nutrition on pancreatic exocrine and endocrine secretion in ruminants: a review.

Because of the unique features of the ruminant digestive system, variations in diet composition and intake produce dramatic changes in ruminal fermentation. Optimizing nutritional management requires an understanding of how these variations and changes influence digestion and metabolism. Although the pancreas plays a central role in digestion and subsequent nutrient metabolism, relatively little is known about pancreatic adaptation to nutritional changes in the ruminant. Increasing starch intake has been suggested to increase pancreatic alpha-amylase; however, recent work suggests that dietary energy per se may drive these changes, and interactions with other nutrients, such as protein, may exist. Studies describing the influence of altered protein and lipid intakes on pancreatic adaptation in ruminants are lacking. Pancreatic secretion of both insulin and glucagon respond to the intravenous infusion of VFA in a dramatic fashion; however, feeding studies suggest that the influence of VFA on insulin and glucagon may be more subtle. Interactions exist between stimulatory signals and physiological state, such as lactation. Assessment of pancreatic endocrine secretion is further complicated by a variable removal of insulin and glucagon by hepatic tissues. These studies point out that pancreatic hormone secretion is controlled by integrated and complex mechanisms. Studies of these controlling mechanisms should consider the entire array to more fully understand hormone secretion.     

Effect of triglycerides on growth hormone (GH)-releasing factor-mediated GH secretion in newborn calves

The effect of triglycerides (Tg) on GRF-mediated GH secretion was examined in 2 groups of twelve ten-day old male calves. Twelve calves were intravenously infused with a lipid-heparin solution (5 mg Tg and 0.3 IU heparin/kg body wt/min for 90 min). The twelve control calves received in the same way, the same volume of saline. Thirty minutes after the start of infusion, GRF 1–29 (human amide, 0.16 μg/kg body wt) was intravenously injected in six animals of each group.

Mean plasma GH levels reached peak concentrations in the 2 groups 5 min after GRF injection. However the area under the GH response curve, when lipid-heparin was given, was significantly diminished compared to the response when saline was given. In the same time, lipid-heparin treatment increased plasma SRIF concentration. These data suggest that an increase in plasma Tg concentration, induced by lipid-heparin infusion, inhibits GRF-mediated GH secretion, possibly through stimulation of SRIF secretion.     

Effect of volatile fatty acid infusion on blood plasma free amino acid profiles in growing lambs.

Five ram lambs (average body mass: 25 kg) were given, through a catheter inserted into the left ruminal vein, a total of 28.8 mM sodium acetate, 14.4 mM sodium propionate and 4.8 mM sodium butyrate per kg body mass as a 2-hour infusion. During and at 0, 1, 2, 4, 6, 10 and 24 h after the infusion blood samples were taken from the jugular vein and the blood plasma was assayed for free amino acid (FAA) and immunoreactive insulin (IRI) concentrations. Volatile fatty acid (VFA) infusion significantly decreased the blood plasma concentrations of all FAA but cystine. The lowest FAA concentrations were measured in plasma samples taken at the end of the 2-h infusion. Subsequently the level of all amino acids rose and by 24 h after the infusion the blood plasma concentration of all FAA came close to the preinfusion value. The largest differences were observed in the concentration of glutamate, glycine, leucine and isoleucine. In contrast to FAA, IRI concentration was increased significantly (almost fivefold) by VFA infusion. By 10 h after the infusion IRI concentration returned to the initial level. The results reported here indicate that energy supply given in the form of VFA infusion significantly affects blood plasma FAA profiles, supposedly as a result of changes induced in protein synthesis in tissues. Insulin presumably plays a role in the regulation of these changes.     

Effects of glucose and amino acids on ghrelin secretion in sheep

Two experiments were conducted to elucidate the effects of post‐ruminal administration of starch and casein (Exp. 1), plasma amino acids concentrations (Exp. 2), and plasma glucose and insulin concentrations (Exp. 2) on plasma ghrelin concentrations in sheep. In Exp. 1, plasma ghrelin concentrations were determined by four infusion treatments (water, cornstarch, casein and cornstarch plus casein) in four wethers. Abomasal infusion of casein increased plasma α‐amino N (AAN) concentrations. Infusion of starch or casein alone did not affect plasma ghrelin concentrations, but starch plus casein infusion increased plasma levels of ghrelin, glucose and AAN. In Exp 2, we investigated the effects of saline or amino acids on ghrelin secretion in four wethers. Two hours after the initiation of saline or amino acid infusion into the jugular vein, glucose was also continuously infused to investigate the effects of blood glucose and insulin by hyper‐glycemic clump on plasma ghrelin concentrations. Infusion of amino acids alone raised plasma levels of ghrelin, but the higher plasma glucose and insulin concentrations had no effect on plasma ghrelin concentrations. These results suggest that high plasma levels of amino acids can stimulate ghrelin secretion, but glucose and insulin do not affect ghrelin secretion in sheep.     

Effect in sheep of dietary concentrate content on secretion of growth hormone, insulin and insulin-like growth factor-I after feeding

This study was designed to examine the effects of the proportion of concentrate in the diet on the secretion of growth hormone (GH), insulin and insulin‐like growth factor‐I (IGF‐I) secretion and the GH‐releasing hormone (GHRH)‐induced GH response in adult sheep fed once daily. Dietary treatments were roughage and concentrate at ratios of 100:0 (0% concentrate diet), 60:40 (40% concentrate diet), and 20:80 (80% concentrate diet) on a dry matter basis. Mean plasma concentrations of GH before daily feeding (10.00–14.00 hours) were 11.4 ± 0.4, 10.1 ± 0.5 and 7.5 ± 0.3 ng/mL on the 0, 40 and 80% concentrate diet treatments, respectively. A significant decrease in plasma GH concentration was observed after daily feeding of any of the dietary treatments and these decreased levels were maintained for 8 h (0%), 12 h (40%) and 12 h (80%), respectively (P < 0.05). Plasma IGF‐I concentrations were significantly decreased 8–12 h and 4–16 h after the end of feeding compared with the prefeeding level in the 40 and 80% concentrate diet treatments, respectively (P < 0.05). GHRH injection brought an abrupt increase in the plasma GH concentrations, reaching a peak 10 min after each injection, but, after the meal, the peak plasma GH values for animals fed 40% (P < 0.05) and 80% (P < 0.01) concentrate diet were lower than that for roughage fed animals. The concentrate content of a diet affects the anterior pituitary function of sheep resulting in reduced baseline concentrations of GH and prolonged GH reduction after feeding once daily.     

Growth hormone secretion and pancreatic function following somatostatin infusion in ducks (Anas platyrhynchos)

The intravenous infusion of somatostatin (800 ng/kg min) reduced the concentration of growth hormone (GH) in the plasma of 4 to 5, 6 to 7 and 8 to 9 week-old ducklings, but not in adult ducks. The inhibition of GH secretion was not due to accompanying changes in pancreatic function, since the infusion of a lower dose of somatostatin (200 ng/kg min) increased glucagon release and decreased plasma free fatty acids (FFA), as observed with the higher dose, but had no effect on GH concentrations. The withdrawal of somatostatin inhibition resulted in rebound GH secretion in immature birds, the magnitude of which was directly related to the pre-treatment level. Following somatostatin infusion (800 ng/kg min) no modification in GH concentration was observed in adult ducks. These results demonstrate that basal GH release in young birds is not autonomous and is suppressible by somatostatin. The data provide further evidence for age-related changes in the control of avian GH and insulin release and for the independence of the effects of somatostatin on the pituitary and pancreas glands.     

Serum leptin concentrations, luteinizing hormone and growth hormone secretion during feed and metabolic fuel restriction in the prepuberal gilt

Two experiments were conducted to determine 1) the effect of acute feed deprivation on leptin secretion and 2) if the effect of metabolic fuel restriction on LH and GH secretion is associated with changes in serum leptin concentrations. Experiment (EXP) I, seven crossbred prepuberal gilts, 66 +/- 1 kg body weight (BW) and 130 d of age were used. All pigs were fed ad libitum. On the day of the EXP, feed was removed from four of the pigs at 0800 (time = 0) and pigs remained without feed for 28 hr. Blood samples were collected every 10 min from zero to 4 hr = Period (P) 1, 12 to 16 hr = P 2, and 24 to 28 hr = P 3 after feed removal. At hr 28 fasted animals were presented with feed and blood samples collected for an additional 2 hr = P 4. EXP II, gilts, averaging 140 d of age (n = 15) and which had been ovariectomized, were individually penned in an environmentally controlled building and exposed to a constant ambient temperature of 22 C and 12:12 hr light: dark photoperiod. Pigs were fed daily at 0700 hr. Gilts were randomly assigned to the following treatments: saline (S, n = 7), 100 (n = 4), or 300 (n = 4) mg/kg BW of 2-deoxy-D-glucose (2DG), a competitive inhibitor of glycolysis, in saline iv. Blood samples were collected every 15 min for 2 hr before and 5 hr after treatment. Blood samples from EXP I and II were assayed for LH, GH and leptin by RIA. Selected samples were quantified for glucose, insulin and free fatty acids (FFA). In EXP I, fasting reduced (P < 0.04) leptin pulse frequency by P 3. Plasma glucose concentrations were reduced (P < 0.02) throughout the fast compared to fed animals, where as serum insulin concentrations did not decrease (P < 0.02) until P 3. Serum FFA concentrations increased (P < 0.02) by P 2 and remained elevated. Subcutaneous back fat thickness was similar among pigs. Serum IGF-I concentration decreased (P < 0.01) by P 2 in fasted animals compared to fed animals and remained lower through periods 3 and 4. Serum LH and GH concentrations were not effected by fast. Realimentation resulted in a marked increase in serum glucose (P < 0.02), insulin (P < 0.02), serum GH (P < 0.01) concentrations and leptin pulse frequency (P < 0.01). EXP II treatment did not alter serum insulin levels but increased (P < 0.01) plasma glucose concentrations in the 300 mg 2DG group. Serum leptin concentrations were 4.0 +/- 0.1, 2.8 +/- 0.2, and 4.9 +/- 0.2 ng/ml for S, 100 and 300 mg 2DG pigs respectively, prior to treatment and remained unchanged following treatment. Serum IGF-I concentrations were not effected by treatment. The 300 mg dose of 2DG increased (P < 0.0001) mean GH concentrations (2.0 +/- 0.2 ng/ml) compared to S (0.8 +/- 0.2 ng/ml) and 100 mg 2DG (0.7 +/- 0.2 ng/ml). Frequency and amplitude of GH pulses were unaffected. However, number of LH pulses/5 hr were decreased (P < 0.01) by the 300 mg dose of 2DG (1.8 +/- 0.5) compared to S (4.0 +/- 0.4) and the 100 mg dose of 2DG (4.5 +/- 0.5). Mean serum LH concentrations and amplitude of LH pulses were unaffected. These results suggest that acute effects of energy deprivation on LH and GH secretion are independent of changes in serum leptin concentrations.     

Basal and Glucagon-Stimulated Plasma C-PeDtide Concentrations in Healthy Dogs, Dogs With Diabetes Millitus, and Dogs With Hyperadrenocorticism

Serum glucose and plasma C-peptide response to IV glucagon administration was evaluated in 24 healthy dogs, 12 dogs with untreated diabetes mellitus, 30 dogs with insulin-treated diabetes mellitus, and 8 dogs with naturally acquired hyperadrenocorticism. Serum insulin response also was evaluated in all dogs, except 20 insulin-treated diabetic dogs. Blood samples for serum glucose, serum insulin, and plasma C-peptide determinations were collected immediately before and 5,10,20,30, and (for healthy dogs) 60 minutes after IV administration of 1 mg glucagon per dog. In healthy dogs, the patterns of glucagon-stimulated changes in plasma C-peptide and serum insulin concentrations were identical, with single peaks in plasma C-peptide and serum insulin concentrations observed approximately 15 minutes after IV glucagon administration. Mean plasma C-peptide and serum insulin concentrations in untreated diabetic dogs, and mean plasma C-peptide concentration in insulin-treated diabetic dogs did not increase significantly after IV glucagon administration. The validity of serum insulin concentration results was questionable in 10 insulin-treated diabetic dogs, possibly because of anti-insulin antibody interference with the insulin radioimmunoassay. Plasma C-peptide and serum insulin concentrations were significantly increased (P < .001) at all blood sarnplkg times after glucagon administration in dogs with hyperadrenocorticism, compared with healthy dogs, and untreated and insulin-treated diabetic dogs. Five-minute C-peptide increment, C-peptide peak response, total C-peptide secretion, and, for untreated diabetic dogs, insulin peak response and total insulin secretion were significantly lower (P < .001) in diabetic dogs, compared with healthy dogs, whereas these same parameters were significantly increased (P < .011 in dogs with hyperadrenocorticism, compared with healthy dogs, and untreated and insulin-treated diabetic dogs. Although not statistically significant, there was a trend for higher plasma C-peptide concentrations in untreated diabetic dogs compared with insulin-treated diabetic dogs during the glucagon stimulation test. Baseline C-peptide concentrations also were significantly higher (P < .05) in diabetic dogs treated with insulin for less than 6 months, compared with diabetic dogs treated for longer than 1 year. Finally, 7 of 42 diabetic dogs had baseline plasma C-peptide concentrations greater than 2 SD (ie, >0.29 pmol/mL) above the normal mean plasma C-peptide concentration; values that were significantly higher, compared with results in healthy dogs (P < .001) and with the other 35 diabetic dogs (P < .001). In summary, measurement of plasma C-peptide concentration during glucagon stimulation testing allowed differentiation among healthy dogs, dogs with impaired β-cell function (ie, diabetes mellitusl, and dogs with increased β-cell responsiveness to glucagon (ie, insulin resistance). Plasma C-peptide concentrations during glucagon stimulation testing were variable in diabetic dogs and may represent dogs with type-1 and type-2 diabetes or, more likely, differences in severity of β-cell loss in dogs with type-1 diabetes. J Vet Intern Med 1996;10:116–122. Copyright © 1996 by the American College of Veterinary Internal Medicine.     

Pancreatic exocrine secretion and plasma concentration of some gastrointestinal hormones in response to abomasal infusion of starch hydrolyzate and/or casein

Eight Angus steers (290 +/- 8 kg), surgically prepared with pancreatic pouch-duodenal reentrant cannulas and abomasal infusion catheters were used in a replicated 4 x 4 Latin square experiment to investigate the effects of abomasal infusion of starch hydrolyzate (SH) and/or casein on pancreatic exocrine secretion and plasma concentration of hormones. Steers were fed a basal diet of alfalfa (1.2 x NEm) in 12 equal portions daily. Abomasal infusion treatments (6-L total volume infused per day) were water (control), SH [2.7 g/(kg BW x d)], casein [0.6 g/(kg BW x d)], and SH + casein. Periods were 3 d for adaptation and 8 d of full infusion. Pancreatic juice and jugular blood samples were collected over 30-min intervals for 6 h on d 11. Weight and pH of pancreatic samples were measured, and a 10% subsample was composited and frozen until analysis of total protein and pancreatic enzyme activities. The remaining sample was returned to the duodenum. Plasma was harvested and frozen until analyzed. Pancreatic juice (67 mL/h) and protein (1.8 g/h) secretion rates were not affected by nutrient infusion. There were SH x casein interactions for all pancreatic enzyme secretions (U/h; alpha-amylase, P < 0.03; trypsin, P < 0.08; and chymotrypsin, P < 0.03) and plasma insulin concentration (P < 0.10). Secretion of pancreatic enzymes was increased by SH (trypsin) and casein (alpha-amylase, trypsin, and chymotrypsin) but not when SH + casein were infused together. Glucose (P < 0.10) and cholecystokinin octapeptide concentrations (CCK-8; P < 0.05) were increased by SH, but glucagon was decreased (P < 0.10). Casein decreased (P < 0.10) plasma CCK-8 concentrations. These data indicate that positive effects of postruminal casein on enzyme secretion were inhibited by SH, emphasizing the complexity of the regulatory mechanisms involved in dietary adaptation of pancreatic exocrine secretion. Changes in hormone concentration may not relate directly to changes in enzyme secretion.     

Depression of hyperglycemic response to glucagon by parenteral lead administration in sheep.

The insulin and glucose responses to glucagon infusions (27 microgram/hr) were determined in sheep before and after parenteral lead treatment (6 mg/kg intravenously). Glucose production was measured by primed continuous infusion of [6-3H]glucose. Glucagon and insulin concentrations before and during glucagon infusions were not significantly different between lead treatment and control experiments. Lead administration did not affect the concentration or production of glucose in the preinfusion period. However, depressed hyperglycemia during glucagon infusion in lead treated experiments tended to be associated with decreased glucose production. The reduced glucogenic response to glucagon may be the result of reduced function of pyruvate carboxylase, a key hepatic gluconeogenic enzyme in sheep, from lead induced impairment of mitochondrial function.     

灌注果寡糖对生长绵羊瘤胃发酵功能的影响

采用营养灌注技术研究了果寡糖对生长绵羊瘤胃发酵功能的影响。试验选取6只安装有永久性瘤胃瘘管的内蒙古半细毛羯羊，随机分为两组，试验组一灌注1．00％果寡糖，试验组二灌注2．00％果寡糖。结果表明：灌注果寡糖可以显著（P〈0．05）降低试羊的瘤胃液相pH和瘤胃内的NH3-N浓度，显著提高（P〈0．05）瘤胃内的VFA含量和MCP含量。两个灌注水平都可以提高生长绵羊的瘤胃发酵功能。但2．00％的灌注水平仅在瘤胃NH3-N浓度的降幅方面比1．00％的灌注水平显著增大（P〈0．05），在对瘤胃液相pH值、VFA含量和MCP含量的影响方面两个灌注水平没有显著差异（P〉0．05）。     

Feeding-induced increases in insulin do not suppress secretion of growth hormone

Secretion of growth hormone (GH) is reduced for several hours after feeding when access to feed is restricted to a 2-hr period each day. We hypothesized that increased secretion of insulin after feeding inhibits release of GH from the anterior pituitary gland. Our objectives were to determine whether: 1) alloxan prevents concentrations of insulin from increasing after feeding steers; 2) concentrations of GH remain high after feeding alloxan-treated steers; and 3) GH-releasing hormone (GHRH) stimulates greater release of GH in alloxan-treated, than in control, steers after feeding. Steers were injected iv with either saline (control) or with alloxan (110 mg/kg) (n = 4 per group). Concentrations of insulin were not different (P = 0.61) between control and alloxan-treated steers before feeding (87.5 +/- 33.6 pmol/l). However, alloxan prevented insulin from increasing (P < 0.001) after feeding (131.8 pmol/1) compared with control steers (442.0 pmol/l) (pooled SEM = 47.5). Overall, GH was higher (P < 0.05) in alloxan-treated (6.4 ng/ml) than in control steers (3.7 ng/ml) (pooled SEM = 0.7), but GH decreased (P < 0.001) after feeding in both groups. Iv injection of GHRH stimulated release of GH 1 hr before, but not when injected 1 hr after feeding (P < 0.001). In addition, net areas under the GH curve were not significantly different between control and alloxan-treated groups. We conclude that increased concentrations of insulin after feeding do not mediate feeding-induced suppression of GH secretion in steers.