Subclinical (SCK) and clinical (CK) ketosis are metabolic disorders responsible for big losses in dairy production. Although Fourier-transform mid-infrared spectrometry (FTIR) to predict ketosis in cows exposed to great metabolic stress was studied extensively, little is known about its suitability in predicting hyperketonemia using individual samples, e.g. in small dairy herds or when only few animals are at risk of ketosis. The objective of the present research was to determine the applicability of milk metabolites predicted by FTIR spectrometry in the individual screening for ketosis. In experiment 1, blood and milk samples were taken every two weeks after calving from Holstein (n = 80), Brown Swiss (n = 72) and Swiss Fleckvieh (n = 58) cows. In experiment 2, cows diagnosed with CK (n = 474) and 420 samples with blood β-hydroxybutyrate [BHB] <1.0 mmol/l were used to investigate if CK could be detected by FTIR-predicted BHB and acetone from a preceding milk control. In experiment 3, correlations between data from an in farm automatic milk analyser and FTIR-predicted BHB and acetone from the monthly milk controls were evaluated. Hyperketonemia occurred in majority during the first eight weeks of lactation. Correlations between blood BHB and FTIR-predicted BHB and acetone were low (r = 0.37 and 0.12, respectively, P < 0.0001), as well as the percentage of true positive values (11.9 and 16.6%, respectively). No association of FTIR predicted ketone bodies with the interval of milk sampling relative to CK diagnosis was found. Data obtained from the automatic milk analyser were moderately correlated with the same day FTIR-predicted BHB analysis (r = 0.61). In conclusion, the low correlations with blood BHB and the small number of true positive samples discourage the use of milk mid-infrared spectrometry analyses as the only method to predict hyperketonemia at the individual cow level.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1017/S0022029920000230 | DOI Listing |
During type 1 diabetes (T1D) progression, beta cells become dysfunctional and exhibit reduced first-phase insulin release. While this period of beta cell dysfunction is well established, its cause and underlying mechanism remain unknown. To address this knowledge gap, live human pancreas tissue slices were prepared from autoantibody- negative organ donors without diabetes (ND), donors positive for one or more islet autoantibodies (AAb+), and donors with T1D within 0-4 years of diagnosis (T1D+).
View Article and Find Full Text PDFExposure to saturated fatty acids (SFAs), such as palmitic acid, can lead to cellular metabolic dysfunction known as lipotoxicity. Although canonical adaptive metabolic processes like lipid storage or desaturation are known cellular responses to saturated fat exposure, the link between SFA metabolism and organellar biology remains an area of active inquiry. We performed a genome-wide CRISPR knockout screen in human epithelial cells to identify modulators of SFA toxicity.
View Article and Find Full Text PDFMicrobes of nearly every species can form biofilms, communities of cells bound together by a self-produced matrix. It is not understood how variation at the cellular level impacts putatively beneficial, colony-level behaviors, such as cell-to-cell signaling. Here we investigate this problem with an agent-based computational model of metabolically driven electrochemical signaling in Bacillus subtilis biofilms.
View Article and Find Full Text PDFThe capsaicin receptor, TRPV1, mediates the detection of harmful chemical and thermal stimuli. Overactivation of TRPV1 can lead to cellular damage or death through excitotoxicity, a phenomenon associated with painful neuropathy and the paradoxical use of capsaicin as an analgesic. We exploited capsaicin-evoked death to conduct a systematic analysis of excitotoxicity through a genome-wide CRISPRi screen, thereby revealing a comprehensive network of regulatory pathways.
View Article and Find Full Text PDFMetabolic differences between males and females have been well documented across many species. However, the molecular basis of these differences and how they impact tolerance to nutrient deprivation is still under investigation. In this work, we use to demonstrate that sex-specific differences in fat tissue metabolism are driven, in part, by dimorphic expression of the Integrated Stress Response (ISR) transcription factor, ATF4.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!