PSII-19 The Effects of Maternal Programming on Dairy Bull Calf Response to an Intravenous Glucose Tolerance Test

Calves are prone to health issues with high mortality observed during the first 3 weeks of life. We hypothesized that dam milk production levels and/or mastitis infection during gestation will lead to reduced insulin production and increased circulating glucose concentration in response to an Intravenous Glucose Tolerance Test (IVGTT) in young dairy bull calves. Calves (n = 45) were selected from dams classified has high producers (HI; Top 25% for herd M305; n = 7), high producers with high somatic cell count (SCC; HIMAST; SCC test during gestation over 200,000 cells/mL; n = 15), moderate producers (MOD; lower 60% for herd M305; n =17) or moderate producers with high SCC (MODMAST; n = 6). IVGTT were performed on the calves at 7 weeks of age. Blood samples were collected prior to (-30, -15 and 0 min) infusion of glucose. After glucose (0.15 grams /kg bw) administration, samples were collected at 2, 5, 10, 15, 30, 60, and 120-minutes post infusion. Serum insulin and glucose concentrations were determined at Cornell Veterinary Medical Diagnostic Laboratory (Ithica, NY). Data were analysed in SAS using Proc Mixed. Insulin:glucose ratio was analysed using Proc Mixed with repeated measures for treatment x time. No effect of maternal milk production and/or mastitis infection during gestation was observed on calf baseline insulin, insulin AUC, baseline glucose or glucose AUC (P ≥ 0.12). Similarly, no difference in Insulin:Glucose ratio was observed in these calves (P = 0.66). In conclusion, high maternal milk production and/or mastitis infection may not have an effect on circulating insulin production in calves in response to an IVGTT. Correlation analyses will be performed on these data, as well as additional analyses, to determine if insulin sensitivity or response (ie: phase 1 response) was altered further.

Arterial Platelet Adhesion in Atherosclerosis‐Prone Arteries of Obese, Insulin‐Resistant Nonhuman Primates

Background Platelet–endothelial interactions are thought to contribute to early atherogenesis. These interactions are potentiated by oxidative stress. We used in vivo molecular imaging to test the hypothesis that platelet–endothelial interactions occur at early stages of plaque development in obese, insulin‐resistant nonhuman primates, and are suppressed by NADPH‐oxidase‐2 inhibition. Methods and Results Six adult rhesus macaques fed a Western‐style diet for a median of 4.0 years were studied at baseline and after 8 weeks of therapy with the NADPH‐oxidase‐2‐inhibitor apocynin (50 mg/kg per day). Six lean control animals were also studied. Measurements included intravenous glucose tolerance test, body composition by dual‐energy X‐ray absorptiometry, carotid intimal medial thickness, carotid artery contrast ultrasound molecular imaging for platelet GPIbα (glycoprotein‐ Ibα) and vascular cell adhesion molecule‐1, and blood oxidative markers on mass spectrometry. Compared with lean controls, animals on a Western‐style diet were obese (median body mass: 16.0 versus 8.7 kg, P =0.003; median truncal fat: 49% versus 20%, P =0.002), were insulin resistant (4‐fold higher insulin–glucose area under the curve on intravenous glucose tolerance test, P =0.002), had 40% larger carotid intimal medial thickness ( P =0.004), and exhibited oxidative signatures on proteomics. In obese but not lean animals, signal enhancement on molecular imaging was significantly elevated for GPIbα and vascular cell adhesion molecule‐1. The signal correlated modestly with intimal medial thickness but not with the degree of insulin resistance. Apocynin significantly ( P <0.01) reduced median signal for GPIbα by >80% and vascular cell adhesion molecule‐1 signal by 75%, but did not affect intimal medial thickness, body mass, or intravenous glucose tolerance test results. Conclusion In nonhuman primates, diet‐induced obesity and insulin resistance leads to platelet–endothelial adhesion at early atherosclerotic lesion sites, which is associated with the expression of pro‐inflammatory adhesion molecules. These responses appear to be mediated, in part, through oxidative pathways.

Characteristics of Endocrine Metabolism in AL Amyloidosis Patients

Background To explore characteristics of thyroid gland and glucose metabolism in light chain (AL) amyloidosis patients.Methods A total of 20 amyloidosis patients were recruited. Thyroid function and biochemical indices were tested. Intravenous glucose tolerance test was performed in all patients. Thyroid ultrasound was also determined.Results 1.There was 7 patients with hypothyroidism (35%) and 4 patients with subclinical hypothyroidism (20%). Additionally, a total of 6 patients manifested as euthyroid sick syndrome (30%); 2. A number of 15 patients showed thyroid nodule (75%); 3. The fast blood glucose was 4.85±0.8 mmol/l. The level of blood glucose after intravenous glucose tolerance test showed 8.03±1.88 mmol/l at 30 minutes and 7.1±3.22 mmol/l at 120 minutes. 4. The blood insulin levels in fasting, 30 minutes and 120 minutes were 5.2±2.59 mIU/L, 308.3±199.4 mIU/Land 245.66±176.44 mIU/L. Further, the values of C-peptide showed 2.47±1.43 ng/ml, 6.74±3.16 ng/ml and 8.98±4.83 ng/ml. Homeostasis model assessment of insulin resistance and Homeostasis model assessment of β cells of the patients were 1.2±0.62 and 88.45±46.17, respectively. There were 2 patients diagnosed with diabetes and 1 patient with impaired glucose tolerance.Conclusions AL amyloidosis patients revealed high prevalence of hypothyroidism, subclinical hypothyroidism and euthyroid sick syndrome. However, glucose metabolism showed no influence in amyloidosis patients.