Effects of a four-day hyperinsulinemic-euglycemic clamp in early and mid-lactation dairy cows on plasma concentrations of metabolites, hormones, and binding proteins.

The effects of insulin, using a 4 d hyperinsulinemic-euglycemic clamp, on plasma concentrations of hormone, metabolites, and binding proteins were evaluated in four Holstein dairy cows during wk 4 and 17 of lactation. Insulin was infused at 1 microg/kg/hr for 96 hr during the clamp period. Compared with the pre-clamp period, plasma insulin concentrations increased 7-fold and 4-fold during the clamp periods in early and mid-lactation, respectively. The total amount of glucose infused was higher (P < 0.05) during the clamp in early lactation. The clamp decreased plasma concentrations of non-esterified fatty acids (P < 0.001) during early lactation while differences in mid-lactation were minor. The clamp also decreased plasma concentration of beta-hydroxybutyrate (P < 0.001), plasma urea nitrogen (P < 0.001), and true protein (P < 0.01) although the patterns of decline differed between early and mid-lactation. Growth hormone (GH) concentrations decreased (P < 0.001) and insulin-like growth factor-1 (IGF-1) increased (P < 0.01) during the clamp period suggesting a direct effect of insulin on the un-coupling of the GH/IGF-1 axis. Levels of IGF binding protein-2 (IGFBP-2) decreased (P < 0.01) during the clamp period. The relative proportion of IGFBP-2 decreased (P < 0.001) and that of IGFBP-3 increased (P < 0.001) during the clamp period. There were no interactions between the clamp period and stage of lactation on GH, IGF-1, or IGFBPs. Overall, most plasma variables measured were affected in the same way during the two clamps, but the pattern of change often varied with stage of lactation.     

Effects of carnitine and taurine on fatty acid metabolism and lipid accumulation in the liver of cats during weight gain and weight loss

OBJECTIVE: To determine the effects of carnitine (Ca) or taurine (Ta) supplementation on prevention of lipid accumulation in the liver of cats. ANIMALS: 24 adult cats. PROCEDURE: Cats were fed a weight-gaining diet sufficient in n-6 polyunsaturated fatty acids (PUFAs), low in long-chain n-3 PUFAs (n-3 LPUFA), and containing corn gluten for 20 weeks. Cats gained at least 30% in body weight and were assigned to 4 weight-reduction diets (6 cats/diet) for 7 to 10 weeks (control diet, control plus Ca, control plus Ta, and control plus Ca and Ta). RESULTS: Hepatic lipids accumulated significantly during weight gain and weight loss but were not altered by Ca orTa after weight loss. Carnitine significantly increased n-3 and n-6 LPUFAs in hepatic triglycerides, decreased incorporation of 13C palmitate into very-low-density lipoprotein and hepatic triglycerides, and increased plasma ketone bodies. Carnitine also significantly increased weight loss but without altering the fat to lean body mass ratio. Taurine did not significantly affect any variables. Diets low in n-3 LPUFAs predisposed cats to hepatic lipidosis during weight gain, which was further exacerbated during weight loss. Mitochondrial numbers decreased during weight gain and weight loss but were not affected by treatment. Carnitine improved fatty acid oxidation and glucose utilization during weight loss without correcting hepatic lipidosis. CONCLUSIONS AND CLINICAL RELEVANCE: The primary mechanism leading to hepatic lipidosis in cats appears to be decreased fatty acid oxidation. Carnitine may improve fatty acid oxidation but will not ameliorate hepatic lipidosis in cats fed a diet low in n-3 fatty acids.     

Metabolic and hormonal alterations in cats with hepatic lipidosis

Hepatic lipidosis in cats is a commonly diagnosed hepatobiliary disease of unknown cause. The purpose of this prospective study was to characterize the blood hormone and lipid status of cats with hepatic lipidosis, and to compare this status to that of cats with other types of liver disease and to control cats. Twenty-three cats with hepatic disease were assigned to 1 of 2 groups on the basis of cytopathologic or histopathologic examination of the liver: group 1, hepatic lipidosis (n = 18); or group 2, cholangiohepatitis (n = 5). Ten healthy young adult cats were used as controls. Food was withheld from control animals for 24 hours before blood collection. Concentrations of plasma glucagon and serum insulin, cortisol, thyroxine, triglycerides, cholesterol, phospholipids, and nonesterified fatty acids (NEFAs) were determined in all cats, in addition to routine hematologic and serum biochemical testing. Cats with hepatic lipidosis had higher serum NEFA concentrations than cats with cholangiohepatitis or control cats (P < .05). Cats with cholangiohepatitis had higher serum cholesterol and phospholipid concentrations than those of cats with lipidosis or control cats (P < .05); their plasma glucagon concentrations were higher than those of control cats (P < .05), but were not different from those of cats with hepatic lipidosis. Serum insulin concentrations were significantly higher in control cats than in diseased cats (P < .05), but neither serum insulin nor the insulin to glucagon ratio was significantly different among the cats with hepatic disease. The high concentration of NEFAs in cats with hepatic lipidosis suggests that at least 1 factor in the pathogenesis of this syndrome may involve the regulation of hormone-sensitive lipase.     

The Role of Exogenous Insulin in the Complex of Hepatic Lipidosis and Ketosis Associated with Insulin Resistance Phenomenon in Postpartum Dairy Cattle

As a result of a marked decline in dry matter intake (DMI) prior to parturition and a slow rate of increase in DMI relative to milk production after parturition, dairy cattle experience a negative energy balance. Changes in nutritional and metabolic status during the periparturient period predispose dairy cattle to develop hepatic lipidosis and ketosis. The metabolic profile during early lactation includes low concentrations of serum insulin, plasma glucose, and liver glycogen and high concentrations of serum glucagon, adrenaline, growth hormone, plasma β-hydroxybutyrate and non-esterified fatty acids, and liver triglyceride. Moreover, during late gestation and early lactation, flow of nutrients to fetus and mammary tissues are accorded a high degree of metabolic priority. This priority coincides with lowered responsiveness and sensitivity of extrahepatic tissues to insulin, which presumably plays a key role in development of hepatic lipidosis and ketosis. Hepatic lipidosis and ketosis compromise production, immune function, and fertility. Cows with hepatic lipidosis and ketosis have low tissue responsiveness to insulin owing to ketoacidosis. Insulin has numerous roles in metabolism of carbohydrates, lipids and proteins. Insulin is an anabolic hormone and acts to preserve nutrients as well as being a potent feed intake regulator. In addition to the major replacement therapy to alleviate severity of negative energy balance, administration of insulin with concomitant delivery of dextrose increases efficiency of treatment for hepatic lipidosis and ketosis. However, data on use of insulin to prevent these lipid-related metabolic disorders are limited and it should be investigated.     

Effect of energy density in the diet and milking frequency on hepatic long chain fatty acid oxidation in early lactating dairy cows

The objective of this study was to examine the effects of diet energy density (high versus low) and increased milk yield, induced by increased milking frequency (two versus three times daily), on the hepatic status of triacylglycerol (TAG) and glycogen content and hepatic long chain fatty acid (LCFA) oxidation capacity in early lactation in a 2 x 2 factorial design. Forty multiparous Danish-Holstein dairy cows were used from 8 weeks before to 8 weeks after calving. Liver biopsies and blood samples were taken in weeks -2, 2, and 7 from calving. The cows fed the high energy density diet, compared with the cows fed the low energy density diet, had an 18 and 28% higher milk production and net energy intake, respectively. Milk yield was increased by 10% when the cows were milked three times compared with twice daily. Complete (CO2 production) and incomplete (ketone body production) LCFA oxidation capacity in the liver were 35 and 32% higher, respectively, and liver TAG content was 48% lower for the cows fed the high energy density diet compared with the low energy density diet. Overall there was no effect of milking frequency on liver parameters. However, a significant interaction between diet and milking frequency showed that the cows milked three times daily and fed the low energy density diet had the lowest liver LCFA oxidation (CO2 and ketone body) capacity. Furthermore, these cows had the numerically highest liver TAG content. The results for liver LCFA metabolism are discussed in relation to the plasma concentration of metabolites and insulin. In conclusion, cows in early lactation given a high energy density diet will, in general, have a lower risk of high TAG infiltration in the liver.     

Porcine leptin inhibits lipogenesis in porcine adipocytes

The present study examined whether recombinant porcine leptin alters lipid synthesis in porcine adipocytes. The stromal-vascular cell fraction of neonatal pig subcutaneous adipose tissue was isolated by collagenase digestion, filtration, and subsequent centrifugation. These cells were seeded on 25-cm2 tissue culture flasks and proliferated to confluency in 10% (vol/vol) fetal bovine serum in Dulbecco's modified Eagle medium/F12 (DMEM/F12, 50:50). Cultures were differentiated using 2.5% pig serum (vol/vol), 10 nM insulin, 100 nM hydrocortisone. After 7 d of lipid filling, cultures were washed free of this medium, incubated overnight in DMEM/F12 containing 2% pig serum (vol/vol), and then used for experiments. Acute experiments assessed U-(14)C-glucose or 1-(14)C-palmitate metabolism in cultures exposed to porcine leptin (0 to 1,000 ng/mL medium) for 4 h. Chronic experiments used cultures incubated with 0 to 1,000 ng porcine leptin/mL medium for 44 h before measurements of U-(14)C-glucose and 1-(14)C-palmitate oxidation and incorporation into lipid. Another experiment examined whether chronic leptin treatment alters insulin responsiveness by including insulin (10 nM) with incubations containing leptin. Leptin had no acute effects on glucose oxidation or conversion to lipid (P > 0.05). Acute leptin treatment decreased palmitate incorporation into lipids up to 45% (P < 0.05). Chronic leptin exposure decreased glucose oxidation (21%), total lipid synthesis (18%), and fatty acid synthesis (23%) at 100 ng/mL medium (P < 0.05). Insulin increased rates of glucose oxidation, total lipid, and fatty acid synthesis (P < 0.05); however, chronic exposure to 10 ng leptin/mL medium decreased the effectiveness of 10 nM insulin to affect these measures of glucose metabolism by approximately 18 to 46% (P < 0.05). Higher concentrations of leptin inhibited all effects of insulin on glucose metabolism (P < 0.05). Chronic exposure to leptin increased palmitate oxidation by 36% (P < 0.05). Chronic leptin exposure decreased palmitate incorporation into total lipids by 40% at 100 ng/mL medium (P < 0.05). Lipoprotein lipase activity was not affected (P > 0.05) by leptin. These data indicate that leptin functions to promote partitioning of energy away from lipid accretion within porcine adipose tissue by inhibiting glucose oxidation and lipogenesis indirectly, by decreasing insulin-mediated stimulation of lipogenesis, and by stimulating fatty acid oxidation while inhibiting fatty acid esterification.     

Decrease in stearic acid proportions in adipose tissues and liver lipids in fatty liver of dairy cows

Samples of liver and perirenal, mesenteric and subcutaneous fat were collected from 16 sick necropsied dairy cows to evaluate the fatty acid profiles in the hepatic and adipose tissues associated with advanced fatty liver or hepatic lipidosis. Hepatic triglyceride and eight fatty acids were measured in the hepatic and adipose tissues. Six cows had more than 3% triglyceride on fresh weight in their livers and were classified as having fatty liver. Stearic and linoleic acid proportions in the liver decreased markedly with increased hepatic triglyceride levels, while the proportion of palmitic and oleic acids increased. The most striking fluctuations in hepatic lipidosis were manifested as decreased stearic acid in the adipose tissues including subcutaneous fat with the trend of decreasing stearic acid. Palmitic acid was elevated in hepatic and perirenal fat in fatty liver cows. In instances of advanced hepatic lipidosis, palmitoleic acid increased in only subcutaneous fat and not in perirenal or mesenteric fat. In addition to the proportions of hepatic fatty acids in fatty liver, this study also clarified the fluctuations observed in the profiles of fatty acids of the adipose tissues in cows with advanced hepatic lipidosis, particularly the decline in the proportions of stearic acid.     

日粮添加不同比例的中短链和长链脂肪酸对奶牛免疫功能的影响

为探讨不同比例的中短链和长链脂肪酸混合物对奶牛免疫功能的影响,试验选用72头产奶量、胎次及泌乳日龄相近的中国荷斯坦奶牛,按随机区组试验设计,分为对照组和5个处理组,对照组饲喂基础日粮,处理组在基础日粮上分别添加400 g/d 长链脂肪酸(LCFA,A组)、80 g/d中短链脂肪酸(SMCFA)+320 g/d LCFA(B组)、400 g/d 黄油(C组)、240 g/d SMCFA+160 g/d LCFA(D组)及400 g/d SMCFA(E组)。试验期为63 d,第1周为预试期,试验期最后1 d采集血液样品,用于测定血清中免疫球蛋白及细胞因子的含量。结果显示,日粮添加不同比例的中短链和长链脂肪酸对奶牛血清中免疫球蛋白M(IgM)及前列腺素(PGE₂)的含量没有显著影响(P＞0.05);A组免疫球蛋白A(IgA)的含量显著高于B、E组(P＜0.05),B、D组免疫球蛋白G(IgG)的含量显著高于其余4组(P＜0.05)。日粮中添加脂肪酸均能提高奶牛血清中IL-4及IL-10的含量,尤其是D组,增加效果极显著(P＜0.01)。因此,添加240 g/d SMCFA 和160 g/d LCFA更能提高泌乳中期奶牛的免疫性能。     

Effects of nutrient supply, plasma metabolites, and nutritional status of sows during transition on performance in the next lactation

The aim of the present study was to evaluate the effects of nutrient supply, plasma metabolites, and nutritional status of sows during the transition from gestation to lactation on performance of piglets during the colostral period and throughout lactation. Forty second-parity sows were fed 1 of 4 gestation diets containing a different quantity of dietary fiber (171 to 404 g/kg of DM) from mating until d 108 of gestation. From d 108 of gestation until weaning (d 28 of lactation), sows were fed 1 of 5 lactation diets with a different quantity of dietary fat [3 or 8% with different proportions of medium- (MCFA) and long-chain fatty acids (LCFA)]. Blood was obtained by jugular venipuncture on d 108 and 112 of gestation and on d 1 of lactation, and concentrations of plasma glucose, NEFA, lactate, acetate, propionate, butyrate, and fatty acids were analyzed. Piglet growth and mortality were noted throughout lactation. Piglet mortality during the colostral period (0 to 24 h) was affected by the lactation diets and was positively related to sow backfat (d 108) and plasma lactate (d 112) and negatively related to mean piglet birth weight (P < 0.05). Mean piglet live BW gain (LWG) was recorded in the periods 0 to 24 h, 7 to 10 d, 14 to 17 d, and 17 to 28 d relative to parturition as indirect measures of colostrum yield (0 to 24 h), milk yield in early lactation (d 7 to 10), and at peak lactation (d 14 to 17 and d 17 to 28). Effects of gestation and lactation diets on studied sow traits were tested on selected days during the transition period and the next lactation, and tested statistically on separate days. The LWG in the colostral period was positively correlated with mean piglet birth weight (P < 0.001), plasma concentrations of propionate and MCFA (P < 0.05), and plasma acetate and butyrate (P < 0.1) on d 1 of lactation. The LWG in early lactation was inversely correlated with plasma lactate on d 108 (P < 0.05), plasma glucose on d 112, and backfat thickness on d 108 (P < 0.10). The LWG at peak lactation was positively correlated with MCFA intake of the sow on d 113 to 115 and backfat thickness on d 108 during the transition, and negatively correlated with intake of LCFA and ME intake on d 108 to 112 (P < 0.05). In conclusion, feeding and body condition of sows during the transition from gestation to lactation is important for neonatal piglet survival, lactation performance of sows, and piglet growth during the next lactation.     

Insulin sensitivity during pregnancy, lactation, and postweaning in primiparous gilts

The objectives were to examine changes in the insulin response during pregnancy, lactation, and postweaning in an experiment involving 10 primiparous Landrace x Large White gilts. Gilts were catheterized at 50 d of pregnancy, and tests were conducted at approximately 59 d of pregnancy (midpregnancy; MP), 106 d of pregnancy (end of pregnancy; EP), 17 d of lactation (L), and 9 d after weaning (PW), respectively. Changes in plasma glucose, insulin, and NEFA concentrations were studied after 3 different tests: ingestion of 1.3 kg of feed (meal test); a glucose tolerance test; and 2 euglycemic, hyperinsulinemic clamp tests, in which 20 and 55 ng of insulin x kg of BW(-1) x min(-1) were infused during 150 min. Fasting concentrations of plasma glucose were less during L than during the other stages (P < 0.001). Concentrations of glucose and insulin increased after ingestion of the meal and decreased thereafter. Plasma insulin returned to basal concentrations at all stages, whereas glucose reached basal concentrations before the end of the meal at the PW test only. Postprandial concentrations of plasma glucose and area under the curve for insulin were greater during L than at the other stages (P < 0.05); both tended to be greater during EP than during MP or after weaning. Concentrations of NEFA were greater during L than at other stages before as well as after a meal (P < 0.001). Glucose half-life was greatest during L, least during MP and PW, and intermediate during EP. Compared with other stages, insulin secretion during the tolerance tests seemed to be delayed during L and, to a lesser extent, at EP. Irrespective of insulin dose, glucose infusion rates during the clamps did not differ between MP and PW, and were greater than during EP and L (P < 0.001). Plasma concentrations of NEFA decreased less rapidly during L than during the other stages. Gilts from EP developed a state of insulin resistance that was further accentuated during L. Changes in insulin responsiveness at MP, EP, and L may be an adaptation that allows gilts to acclimate to the increasing demand of glucose by the growing conceptus and the even greater demands of lactation.     

Insulin responsiveness to glucose and tissue responsiveness to insulin in lactating, pregnant, and nonpregnant, nonlactating beef cows

Insulin responsiveness to glucose and tissue responsiveness to insulin, using the hyperglycemic clamp and the hyperinsulinemic euglycemic clamp techniques, were measured in lactating, late pregnant, and nonpregnant, nonlactating (NPNL) beef cows. The glucose infusion rate (GIR) in the hyperglycemic clamp technique was higher (P less than .05). in lactating cows than in NPNL cows. The plateau in plasma insulin concentration (insulin responsiveness) was higher (P less than .05) in lactating cows than in late pregnant and NPNL cows. Pregnant cows tended to have higher GIR and lower plateau in plasma insulin concentration than NPNL cows. In the hyperinsulinemic euglycemic clamp technique, GIR (tissue responsiveness to insulin) was higher (P less than .05) in lactating cows than in late pregnant cows; values for NPNL cows were intermediate. We conclude that insulin responsiveness to glucose and tissue responsiveness to insulin were enhanced during lactation but tended to be decreased during late pregnancy in beef cows.     

Relationship among blood indicators of lipomobilization and hepatic function during early lactation in high-yielding dairy cows

Blood indicators are used as a tool to diagnose metabolic disorders. The present work was conducted to study the relationships among blood indicators of lipomobilization and hepatic function in high-yielding dairy cows. Two groups of Holstein cows were studied: 27 early lactation cows and 14 mid lactation cows from four different herds with similar husbandry characteristics in Galicia, Spain. Blood samples were obtained to measure beta-hydroxybutyrate (BHB), non-esterified fatty acids (NEFA), triglycerides (TG), and the activity of aspartate transaminase (AST) and gamma-glutamyl transferase. Cows in early lactation had higher levels of BHB and NEFA than mid lactation cows. High lipomobilization (NEFA > 400 µmol/L) was detected in 67% and 7% of early lactation and mid lactation cows, respectively, while subclinical ketosis (BHB > 1.2 mmol/L) was detected in 41% and 28% of the early lactation and lactation cows, respectively. TG concentrations were low in all cows suffering subclinical ketosis and in 61% of the cows with high lipomobilization. During early lactation, 30% of cows suffered hepatic lipidosis as detected by levels of AST. Compromised hepatic function was observed in early lactation cows as shown by lower concentrations of glucose, total protein, and urea.     

Nutritional support for treatment of hepatic lipidosis in a llama

A 3-year-old female llama that was 3 months into her first lactation and 10 weeks pregnant was evaluated for anorexia of 24 hours' duration. On physical examination, the llama was in lateral recumbency, bradycardic, tachypneic, and hyperthermic. Palpation per rectum confirmed the presence of a possible dry fecal mass in the spiral colon. A tissue biopsy specimen of the liver was obtained, and histologic examination revealed moderate diffuse lipid accumulation within the hepatocytes. Lactated Ringer's solution was administered for rehydration, and partial parenteral nutrition was then initiated. Hepatic lipidosis is a disease characterized by abnormal accumulation of lipid in the liver and is associated with high mortality in camelids. Anorexia associated with hepatic lipidosis promotes further lipid mobilization and fatty infiltration of the liver. Partial parenteral nutrition with enteral supplementation may be used to maintain adequate energy intake and minimize further lipid mobilization. The distinctive metabolism of camelids may require higher amino acid supplementation relative to nonprotein calories in parenteral solutions than those traditionally provided to other species. Treatment with insulin may be effective     

Effects of body condition score at parturition and postpartum supplemental fat on adipose tissue lipogenic activity of lactating beef cows

Three-year-old Angus x Gelbvieh beef cows nutritionally managed to achieve a BCS of 4 +/- 0.07 (479.3 +/- 36.3 kg of initial BW) or 6 +/- 0.07 (579.6 +/- 53.1 kg of initial BW) at parturition were used in a 2-yr experiment (n = 36/yr) to determine the effects of BCS at parturition and postpartum lipid supplementation on cow adipose tissue lipogenesis. Beginning 3 d postpartum, cows within each BCS were randomly assigned to be fed hay and a low-fat control supplement or supplements with either cracked high-linoleate safflower seeds or cracked high-oleate safflower seeds until d 60 of lactation. Diets were formulated to be isonitrogenous and isocaloric, and safflower seed diets provided 5% DMI as fat. Adipose tissue biopsies were collected near the tail-head region of cows on d 30 and 60 of lactation. Dietary treatment did not affect (P > or = 0.43) adipose tissue lipogenesis. Body condition score at parturition did not affect acetate incorporation into lipid (P = 0.53) or activity of acetyl CoA carboxylase (P = 0.77) or fatty acid synthase (P = 0.18). Lipoprotein lipase activity and palmitate incorporation into triacyl-glycerol tended to be greater (P = 0.06), and palmitate esterification into total acylglycerols was greater (P = 0.01) in cows with a BCS of 4 at parturition. Mean activity of acetyl-CoA carboxylase (P < 0.001), lipoprotein lipase (P = 0.01), and rate of palmitate incorporation into monoacylglycerol (P = 0.02), diacylglycerol (P = 0.001), triacylglycerol (P = 0.003), and total acylglycerols (P = 0.002) were greater at d 30 than d 60, suggesting a greater proclivity for fatty acid biosynthesis and esterification by adipose tissue at d 30 of lactation. Although dietary lipid supplementation did not affect adipose tissue lipogenesis, results suggest that cows with a BCS of 4 at parturition have a greater propensity to deliver exogenously derived fatty acids to the adipocyte surface and incorporate preformed fatty acids into acylglycerols as stored adipocyte lipid. Additionally, cows in early lactation seemed to be able to synthesize and incorporate more fatty acids into stored lipid than cows during peak lactation.     

Studies on hepatic lipidosis and coinciding health and fertility problems of high-producing dairy cows using the "Utrecht fatty liver model of dairy cows". A review

Fatty liver or hepatic lipidosis is a major metabolic disorder of high-producing dairy cows that occurs rather frequently in early lactation and is associated with decreased health, production and fertility. A background section of the review explores reasons why high-producing dairy cows are prone to develop fatty liver post partum. Hepatic lipidosis and coinciding health and fertility problems seriously endanger profitability and longevity of the dairy cow. Results from a great number of earlier epidemiological and clinical studies made it clear that a different approach was needed for elucidation of pathogenesis and etiology of this complex of health problems. There was a need for an adequate animal model in which hepatic lipidosis and production, health and fertility problems could be provoked under controlled conditions. It was hypothesized that overconditioning ante partum and feed restriction post partum might induce lipolysis in adipose tissue and triacylglycerol accumulation in the liver following calving. This consideration formed the basis for the experiments, which resulted in the "Utrecht fatty liver model of dairy cows". In this model, post partum triacylglycerol-lipidosis as well as the whole complex of health and fertility problems are induced under well-controlled conditions. The experimental protocol based on this hypothesis produced in all cases (10 feeding trials with over 150 dairy cattle) the intended result, i.e. all experimental cows developed post partum higher hepatic triacylglycerol concentrations than did control cows. The model was evaluated in biochemical, clinical pathology, immunological, clinical and fertility terms. It turned out that in this model, post partum triacylglycerol-lipidosis as well as the whole complex of health and fertility problems were induced under well-controlled conditions.     

Insulin-dependent whole-body glucose utilization and insulin-responses to glucose in week 9 and week 19 of lactation in dairy cows fed rumen-protected crystalline fat or free fatty acids

Whole-body insulin-dependent glucose utilization and insulin responses to glucose in euglycemic-hyperinsulinemic clamps (EHGC) and in hyperglycemic clamps (HGC) were evaluated in high yielding dairy cows fed rumen-protected fat (triglycerides), free fatty acids, or a starch-rich ration (n = 5 per group) in Week 9 and Week 19 of lactation. The experiment was performed under conditions of nonsignificant differences in energy and protein balances in Week 9 and Week 19 and in the three groups. Basal (pre-infusion) concentrations of glucose were lower (P < 0.05) in Week 9 than in Week 19 of lactation and were higher (P < 0.05) in Week 9 in cows fed free fatty acids than in cows fed the starch-rich ration. In EHGC, glucose infusion rates were similar in Week 9 and Week 19 and in the different groups, indicating similar insulin-dependent glucose utilization. Furthermore, because insulin concentrations in EHGC in Week 9 and Week 19 and in the three groups were very similar, metabolic clearance rates of insulin were not affected by stage of lactation and feeding. In addition, insulin responses to the same glucose increments in HGC were not different in Week 9 and Week 19 and in the three groups, indicating that insulin secretion was not affected by stage of lactation and feeding. In conclusion, insulin secretion, insulin metabolic clearance rate, and insulin-dependent glucose utilization between Week 9 and Week 19 of lactation were stable. Furthermore, feeding rumen-protected triglycerides or free fatty acids did not significantly modify insulin secretion, insulin metabolic clearance rate and glucose-dependent glucose utilization compared with starch-rich feeding.     

Blood parameters in Swedish dairy herds with high or low incidence of displaced abomasum or ketosis

Sixty dairy herds were studied to investigate the association between long-term incidence of displaced abomasum and clinical ketosis and body condition score and blood profiles, including parameters estimating energy metabolism and hepatic lipidosis in the periparturient period and early lactation. Blood samples were taken around parturition and in early lactation from cows without apparent clinical symptoms of metabolic disorders. A difference in metabolism between high and low incidence herds was shown post-partum by a lower metabolic index (the revised Quantitative Insulin Sensitivity Check Index, RQUICKI), and tendencies for higher concentrations of glucose, insulin and non-esterified fatty acids in the high incidence herds. High incidence herds had more cows and produced on average 1400kg energy-corrected milk per cow per year more than the low incidence herds. No differences were found in parameters reflecting liver cell damage. In the first 3weeks post-partum the RQUICKI was a more sensitive marker of herds with a high incidence of displaced abomasum and clinical ketosis than any of the individual parameters, but further research is needed before practical applications of the RQUICKI can be foreseen.     

Hypoglycemia alters pulsatile luteinizing hormone secretion in the postpartum beef cow

This study tested the hypothesis that the increased glucose requirement of lactation had effects that were independent of the suckling-dependent inhibition of postpartum endocrine function in beef cows. Mature Hereford cows were either suckled ad libitum and infused with saline iv (n = 9) from d 2 through 4 (d 0 = jugular catherization on d 32 +/- 3 postpartum); were nonsuckled and infused with saline from d 2 through 4 (n = 10); or were nonsuckled and infused with phlorizin (3 g/d) from d 2 through 4 (n = 10). Nonsuckled cows infused with phlorizin had lower (P less than .05) plasma concentrations of glucose and amino acid nitrogen (AAN) on d 2 compared with pre-infusion levels (d 1), but their metabolic profile returned to levels similar to the suckled cows by d 3 and 4. Nonsuckled cows infused with saline had elevated glucose and insulin and lower AAN and free fatty acids (FFA) on d 3 and 4 compared with pre-weaning (d 1) levels (P less than .05). Nonsuckled cows infused with phlorizin did not show this weaning-induced elevation in glucose and insulin. The number of luteinizing hormone (LH) pulses was not affected by treatment. However, in contrast to the large LH pulses observed in the nonsuckled cows infused with saline, both the suckled cows and the nonsuckled cows treated with phlorizin had more small and fewer large amplitude pulses (P less than .01). Treatment did not affect serum concentrations of follicle stimulating hormone, gonadotropin release in response to gonadotropin releasing hormone (25 micrograms) or the number of cows ovulating by 55 d after calving. We conclude that the increased glucose clearance caused by phlorizin infusion or lactation results in depression of LH pulse amplitude in suckled postpartum beef cows.     

Decreases in serum apolipoprotein B-100 and A-I concentrations in cows with milk fever and downer cows

Milk fever occurring during the peripartum period has been suggested to be caused by fatty liver developed during the nonlactating stage because diseased cows have increased serum concentrations of non-esterified fatty acids (NEFA) and show hepatic lipidosis. In cows with fatty liver and related diseases such as ketosis, serum concentrations of apolipoprotein (apo) B-100 and apoA-I are decreased. The purpose of the present study was to examine whether apoB-100 and apoA-I concentrations are similarly decreased in cows with milk fever. Apolipoprotein concentrations were also measured in cows with downer syndrome, which has been suggested to be related, at least in part, to milk fever. Compared with healthy cows during early lactation, apoB-100 and apoA-I concentrations were decreased in cows with milk fever and also in downer cows. In cows with milk fever, the decreases in apoB-100 and apoA-I concentrations were associated with increased NEFA and decreased cholesterol and phospholipid concentrations. However, in downer cows, serum lipid concentration changes were not as distinct as in cows with milk fever. These results, coupled with previous findings on the decreases in apoB-100 and apoA-I concentrations of cows with fatty liver-related diseases, suggest that fatty liver is involved in the development of milk fever and partly in that of downer cow syndrome.