glycogen and Puerperal-Disorders

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 beta-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.

Topics: Animal Nutritional Physiological Phenomena; Animals; Blood Glucose; Cattle; Cattle Diseases; Energy Metabolism; Female; Glycogen; Hypoglycemic Agents; Insulin; Insulin Resistance; Insulin Secretion; Ketosis; Lactation; Lipid Metabolism; Liver; Parturition; Postpartum Period; Pregnancy; Puerperal Disorders; Signal Transduction; Triglycerides

Thirty-three Holstein cows averaging 687 kg of body weight were allotted 6 wk before the expected date of parturition to 11 groups of 3 cows blocked within parity for similar calving dates to determine the effects of feeding different sources of fatty acids on blood parameters related to fatty liver and profile of fatty acids in plasma and liver. Cows were fed lipid supplements from 6 wk before the expected date of parturition until d 28 of lactation. Cows within each block were assigned to 1 of 3 isonitrogenous and isoenergetic dietary supplements: control with no added lipids (CO); unsaturated lipids supplied as whole flaxseed (FL; 3.3 and 11.0% of the dry matter in prepartum and postpartum diets, respectively); and saturated lipids supplied as Energy Booster (EB; 1.7 and 3.5% of the DM in prepartum and postpartum diets, respectively). Diets EB and FL had similar ether extract concentrations. Multiparous cows fed EB had lower dry matter intake and milk production, higher concentrations of nonesterified fatty acids and beta-hydroxybutyrate in plasma and triglycerides (TG) and total lipids in liver, and lower concentrations of plasma glucose and liver glycogen than those fed FL and CO. Production of 4% fat-corrected milk was similar among treatments. Multiparous cows fed FL had the highest liver concentrations of glycogen on wk 2 and 4 after calving and lowest concentrations of TG on wk 4 after calving. Liver C16:0 relative percentages in multiparous cows increased after calving whereas those of C18:0 decreased. Relative percentages of liver C16:0 were higher in wk 2 and 4 postpartum for multiparous cows fed EB compared with those fed CO and FL; those of C18:0 were lower in wk 4 postpartum for cows fed EB compared with those fed CO and FL. Liver C18:1 relative percentages of multiparous cows increased after calving and were higher in wk 4 for cows fed EB compared with those fed CO and FL. The inverse was observed for liver C18:2 relative percentages. In general, diets had more significant effects on plasma concentrations of nonesterified fatty acids, beta-hydroxybutyrate, and glucose and liver profiles of fatty acids, TG, total lipids, and glycogen of multiparous than primiparous cows. These data suggest that feeding a source of saturated fatty acids increased the risk of fatty liver in the transition cow compared with feeding no lipids or whole flaxseed. Feeding flaxseed compared with no lipids or a source of saturated fatty acids from 6 wk before calvin

Topics: Animals; Blood Glucose; Body Weight; Cattle; Cattle Diseases; Diet; Dietary Supplements; Fatty Acids; Fatty Acids, Nonesterified; Female; Flax; Glycogen; Lactation; Lipid Metabolism; Lipids; Liver; Milk; Pregnancy; Puerperal Disorders; Time Factors

Nutritional management during the dry period may affect susceptibility of cows to metabolic and infectious diseases during the periparturient period. Thirty-five multiparous Holstein cows were used to determine the effect of prepartum intake, postpartum induction of ketosis, and periparturient disorders on metabolic status. Cows were fed a diet from dry-off to parturition at either ad libitum intake or restricted intake [RI; 80% of calculated net energy for lactation (NEL) requirement]. After parturition, all cows were fed a lactation diet. At 4 d in milk (DIM), cows underwent a physical examination and were classified as healthy or having at least one periparturient disorder (PD). Healthy cows were assigned to the control (n = 6) group or the ketosis induction (KI; n = 9) group. Cows with PD were assigned to the PD control (PDC; n = 17) group. Cows in the control and PDC groups were fed for ad libitum intake. Cows in the KI group were fed at 50% of their intake on 4 DIM from 5 to 14 DIM or until signs of clinical ketosis were observed; then, cows were returned to ad libitum intake. During the dry period, ad libitum cows ate more than RI cows; the difference in intake resulted in ad libitum cows that were in positive energy balance (142% of NEL requirement) and RI cows that were in negative energy balance (85% of NEL requirement). Prepartum intake resulted in changes in serum metabolites consistent with plane of nutrition and energy balance. Prepartum intake had no effect on postpartum intake, serum metabolites, or milk yield, but total lipid content of liver at 1 d postpartum was greater for ad libitum cows than for RI cows. The PD cows had lower intake and milk yield during the first 4 DIM than did healthy cows. During the ketosis induction period, KI cows had lower intake, milk yield, and serum glucose concentration but higher concentrations of nonesterified fatty acids and beta-hydroxybutyrate in serum as well as total lipid and triacylglycerol in liver than did control cows. Cows with PD had only modest alterations in metabolic variables in blood and liver compared with healthy cows. The negative effects of PD and KI on metabolic status and milk yield were negligible by 42 DIM, although cows with PD had lower body condition score and BW. Prepartum intake did not affect postpartum metabolic status or milk yield. Periparturient disorders and induction of ketosis negatively affected metabolic status and milk yield during the first 14 DIM.

Topics: 3-Hydroxybutyric Acid; Animal Nutritional Physiological Phenomena; Animals; Blood Glucose; Cattle; Cattle Diseases; Diet; Energy Intake; Energy Metabolism; Fatty Acids; Fatty Acids, Nonesterified; Female; Glycogen; Ketosis; Lactation; Lipids; Liver; Milk; Parturition; Pregnancy; Puerperal Disorders; Triglycerides

Thirty-five multiparous Holstein cows were used to determine the role of mitochondrial carnitine palmitoyltransferase I (CPT I) in liver on peripartal adaptations of fatty acid metabolism. From dry-off to parturition, cows were fed a diet at either ad libitum (n = 17) or restricted intake (RI, 80% of calculated requirements for net energy; n = 18). After parturition, all cows were fed a lactation diet. At 4 d in milk (DIM), cows underwent a physical examination and were classified as healthy (n = 15) or having at least one periparturient disorder (PD; n = 17). Cows in the healthy group were assigned to either a control (n = 6) group or a ketosis induction (KI; n = 9) group. Cows with periparturient disorders were assigned to a third (PDC; n = 17) group. Cows in control and PDC groups were fed for ad libitum intake. Cows in KI were fed at 50% of their respective intake at d 4 postpartum starting from 5 DIM and continuing to signs of clinical ketosis or until 14 DIM; cows then were returned to ad libitum intake. Liver was biopsied at -30 d, 1 d, at signs of clinical ketosis or 14 d, and 28 d relative to parturition. Mitochondria were isolated by differential centrifugation. Activity of CPT I was 5.4 and 7.6 nmol of palmitoylcarnitine formed per min/mg of protein for ad libitum and RI, respectively, at -30 DIM. Sensitivity of CPT I to its inhibitor, malonyl CoA, did not differ between ad libitum and RI cows. Differences in CPT I activity between ad libitum and RI were no longer significant at 1 DIM. Postpartum CPT I activity and malonyl CoA sensitivity at 1 DIM, onset of clinical ketosis or 14 DIM, and 28 DIM were not affected by prepartum intake (ad libitum vs. RI), postpartum health status (healthy vs. PD), or ketosis induction status (control vs. KI vs. PDC). Activity of CPT I was positively correlated with liver total lipid, liver triglyceride, liver triglyceride to glycogen ratio, and serum nonesterified fatty acids. Activity of CPT I and dry matter intake were not correlated. Prepartum intake affected prepartum CPT I activity but not malonyl CoA sensitivity. Neither induction of primary ketosis nor periparturient disorders greatly affected CPT I activity or sensitivity, which indicates that alterations of CPT I may not be a major factor in the etiology of primary ketosis or other periparturient disorders.

Topics: 3-Hydroxybutyric Acid; Animals; Carnitine O-Palmitoyltransferase; Cattle; Cattle Diseases; Diet; Energy Intake; Enzyme Inhibitors; Fatty Acids, Nonesterified; Female; Glycogen; Ketone Bodies; Ketosis; Kinetics; Lipids; Liver; Malonyl Coenzyme A; Mitochondria, Liver; Parturition; Pregnancy; Puerperal Disorders; Triglycerides

Topics: Acid Phosphatase; Alkaline Phosphatase; Endometritis; Enzyme Activation; Female; Glycogen; Humans; Leukocytes; Peroxidases; Pregnancy; Pregnancy Trimester, Third; Puerperal Disorders

Topics: Adult; Autopsy; Cardiac Catheterization; Cardiomyopathies; Cell Nucleus; Cytoplasm; Electrocardiography; Female; Glycogen; Histocytochemistry; Humans; Microscopy, Electron; Mitochondria; Myocardium; Myofibrils; Pregnancy; Puerperal Disorders

Topics: Carbohydrate Metabolism; Female; Glycogen; Humans; Leukocytes; Pre-Eclampsia; Pregnancy; Puerperal Disorders