Veterinary biochemistry examines the molecules and chemical reactions that support animal life—proteins, enzymes, lipids, carbohydrates and nucleic acids—and how their metabolic dynamics determine health and disease. Understanding these processes is essential to interpret biochemical profiles, design nutritional and pharmacological support, and apply diagnostic techniques with clinical rigor. (Nelson & Cox, 2017)
Importance in Veterinary Medicine
The interpretation of blood and fluid tests is grounded in biochemical pathways: enzyme elevations, metabolite alterations or electrolyte imbalances signal specific molecular processes. Knowing these pathways allows clinicians to convert a numeric result into a pathophysiological hypothesis (e.g., cholestasis, hemolysis, renal failure, hyperglycemia due to insulin resistance). (Kaneko et al., 2014)
In addition, biochemistry underpins pharmacokinetics, toxicology and clinical nutrition: bioavailability, hepatic and renal metabolism, and elimination pathways affect drug efficacy and risk, and determine precise nutritional interventions.
1. Fundamentals of Veterinary Biochemistry
Biomolecules operate in networks: enzymes catalyze specific reactions, substrates and cofactors modulate rate and direction, and hormones adjust metabolic activity according to energy needs or stress. These networks form interconnected anabolic and catabolic routes that, together with allosteric and covalent regulation, enable rapid and sustained responses. (Berg et al., 2015)
Homeostasis is maintained by sensors (receptors), integrators (endocrine and nervous systems) and effectors (enzymes and transporters). Animals exhibit metabolic adaptations according to age, nutrition, exercise and disease: for example, the liver shifts gluconeogenic pathways during fasting, and skeletal muscle modifies energy metabolism with training.
2. Brief history and current approach
Veterinary biochemistry has its origins in the late 19th century, when physiologists began studying how internal chemical processes sustained animal life. Early metabolic analyses focused on digestion, energy metabolism and liver function—especially in species of agricultural interest. Pioneering investigations such as Claude Bernard’s work on hepatic glycogenolysis marked the start of biochemical understanding in animals. (Nelson & Cox, 2017)
Throughout the 20th century, as analytical techniques advanced, biochemistry became an essential diagnostic tool. The adoption of spectrophotometry, chromatography and electrophoresis enabled quantification of enzymes and metabolites, transforming the study of hepatic, renal and metabolic diseases across species. Veterinary laboratories began including routine biochemical panels, strengthening the link between basic science and clinical practice. (Kaneko et al., 2014)
Today, veterinary biochemistry integrates molecular biology and digital technology for a more precise assessment of physiological processes. Techniques such as PCR, metabolomics and automated analyzers allow early detection of alterations and the application of personalized treatments. Thus, the discipline has moved from a descriptive approach to a predictive and applied science, now a cornerstone of modern veterinary diagnostics. (Berg et al., 2015)
3. Main biomolecules and metabolic pathways
Plasma proteins (albumin, globulins) reflect nutritional status, hepatic synthetic capacity and inflammation. Serum enzymes (ALT, AST, ALP, GGT, CK) are markers of tissue damage or enzyme induction; interpreting them requires knowledge of tissue origin, half-life and factors that increase activity (drugs, toxins, exercise). (Kaneko et al., 2014)
Clinically, distinguishing between elevation due to cellular injury (e.g., ALT from hepatocytes) and elevation due to cholestasis (GGT, ALP) directs complementary studies (ultrasound, liver function tests) and defines therapeutic urgency.
Glucose is the primary rapid energy source; its homeostasis depends on insulin (uptake and storage) and glucagon (mobilization and gluconeogenesis). In neonates, obesity or stress, regulation changes; conditions such as diabetes mellitus require dynamic tests (fasting glucose, tolerance curves, fructosamine) for diagnosis and monitoring. (Nelson & Cox, 2017)
In ruminants, plasma glucose dynamics differ due to ruminal fermentation and hepatic gluconeogenesis from precursors such as propionate.
Lipids circulate in lipoproteins (VLDL, LDL, HDL) and are essential for membranes and steroid hormones. Excessive fat mobilization during intense fasting, negative energy balance or parturition can cause hepatic lipidosis or ketosis (especially in felines and ruminants). Lipid profiles and related enzymes (e.g., triglycerides) help diagnose and monitor these conditions. (Berg et al., 2015)
Interpretation must consider pre-analytical factors (fasting, handling) and species and breed variations.
DNA and RNA are the basis for molecular diagnostics: PCR, qPCR and sequencing detect pathogens, mutations and expression levels. In addition, signaling pathways (cAMP, MAPK) explain cellular responses to hormones and drugs; their alteration can lead to therapeutic resistance or metabolic dysfunction.
Animal metabolism consists of an integrated network of biochemical reactions that convert nutrients into usable energy. Key pathways include glycolysis, glycogenesis, gluconeogenesis, the Krebs cycle and beta-oxidation, all coordinated to maintain energy homeostasis and adapt to the organism's needs. (Nelson & Cox, 2017)
In glycolysis, glucose is broken down to pyruvate to generate ATP rapidly, while gluconeogenesis allows glucose formation from non-carbohydrate precursors, a process crucial during prolonged fasting. Glycogenesis and glycogenolysis regulate storage and release of glucose depending on the animal’s energy status. (Berg et al., 2015)
The Krebs cycle is the core of energy metabolism where carbohydrates, lipids and amino acids converge to produce CO₂, NADH and ATP. Beta-oxidation of fatty acids is a major energy source in carnivores and during prolonged exercise, while anabolic processes use this energy for protein and lipid synthesis. (Kaneko et al., 2014)
These pathways are regulated by hormonal signals such as insulin, glucagon and cortisol, which modulate metabolism according to diet, stress or physiological state (gestation, lactation or disease). Dysregulation can cause hypoglycemia, ketosis or metabolic acidosis, particularly in ruminants and production animals. (Sjaastad et al., 2016)
4. Diagnostic methods and analytical quality
Biochemical techniques include colorimetric tests, enzymatic assays, immunoassays and chromatographic and spectrometric methods. The method choice depends on sensitivity, specificity and availability. For example, ALT measurement by spectrophotometry is standard in hepatology, while identification of specific metabolites may require liquid chromatography–mass spectrometry (LC-MS). (St. Louis et al., 2018)
Pre-analytical quality (tube type, anticoagulant, time to centrifugation, hemolysis) and analytical quality (calibration, controls) determine result validity. Standardized protocols, internal and external quality controls and clinical correlation are essential to avoid diagnostic errors.
5. Integrated clinical applications
A biochemical profile must be interpreted as a whole: for example, elevated ALT plus increased bilirubin and alkaline phosphatase indicates a hepatic pattern that may correspond to hepatopathy or cholestasis. Combining these findings with ultrasound, clinical signs and, when appropriate, specific tests (bile acids, coagulation) determines the diagnostic plan and urgency. (Kaneko et al., 2014)
Correcting imbalances (hypoglycemia, acid–base disorders, hyponatremia/hypernatremia) should be based on understanding the underlying pathophysiology and calculating safe correction rates (for example, sodium correction speed). In cases of hepatic or renal failure, adjusting protein and electrolyte intake and administering organ-protective therapies improves prognosis. (Nelson & Cox, 2017)
Many toxins affect biochemical pathways (e.g., xylitol causes hypoglycemia and hepatic failure in dogs; organophosphates inhibit cholinesterase). Rapid identification through history, biochemical testing and, if required, specific analyses (toxin levels) enables antidotes, metabolic support and detoxification measures. (Eddleston et al., 2019)
6. Species variations: diagnostic and therapeutic implications
Physiological differences between species affect pharmacokinetics, metabolism and reference intervals. For example: cats have limited hepatic glucuronidation capacity, which increases sensitivity to certain drugs; cows have unique lipid metabolism adaptations during the transition period; dogs and horses differ in the pharmacokinetics of many active compounds. These differences require species-specific reference ranges and adapted treatments according to species, age and production or companionship context. (Sjaastad et al., 2016)
In practice, always consider context (gestation, lactation, training) and tailor biochemical and pharmacological interventions individually.
References
• Nelson, D. L., & Cox, M. M. (2017). Lehninger Principles of Biochemistry (7th ed.). W. H. Freeman.
• Berg, J. M., Tymoczko, J. L., & Stryer, L. (2015). Biochemistry (8th ed.). W. H. Freeman.
• Kaneko, J. J., Harvey, J. W., & Bruss, M. L. (2014). Clinical Biochemistry of Domestic Animals (6th ed.). Academic Press.
• Sjaastad, Ø. V., Hove, K., & Sand, O. (2016). Physiology of Domestic Animals (3rd ed.). CRC Press.
• St. Louis, K. M., et al. (2018). Analytical Methods in Veterinary Clinical Pathology. Journal/Publisher (reference for methods overview).
• Eddleston, M., et al. (2019). Toxicology of Common Veterinary Poisons. (Review article / clinical toxicology reference).