THE ROLE OF METABOLIC DISORDERS IN THE DEVELOPMENT OF LAMINITIS IN HIGH-PRODUCING DAIRY COWS

Аннотация

В данной статье рассматривается этиологическая и патогенетическая роль метаболических нарушений в развитии ламинита у высокопродуктивных молочных коров, завезённых из-за рубежа в Узбекистан. Анализируются такие факторы, как субклинический рубцовый ацидоз (SARA), гиперинсулинемия, эндотоксемия и нарушения липидного обмена, и их влияние на физиологические реакции организма импортированных пород в условиях агроклиматической среды Узбекистана. В статье также предлагаются усовершенствованные стратегии диагностики и профилактики. Представленные данные способствуют сохранению здоровья копыт, стабильной молочной продуктивности и снижению экономических потерь вфермерскиххозяйствах. Ключевые слова: Импортированные коровы, ламинит, метаболические нарушения, SARA,эндотоксемия,инсулин,здоровьекопыт,рацион,адаптация,акклиматизация. Introduction. In recent years, in Uzbekistan’s livestock sector, imported high-yield dairy cattle breeds — particularly Holstein and Ayrshire breeds brought from the Netherlands, Germany, the USA, and Russia — have been widely reared. However, these animals, which have not fully adapted to local agro-climatic conditions and feeding systems, are commonly affected by hoof diseases, especially laminitis. Laminitis is a disease that damages the connective structures between the hoof wall and the lamellar tissues, leading to impaired locomotion, a sharp decline in milk production, and reduced reproductive performance. This disease frequently occurs in high-producing dairy cows against the background of metabolic stress. Local scientific observations (Karimov B.T., 2023) and international studies (Lean et al., 2013; Goff, 2006) indicate that metabolic disorders — particularly subclinical acidosis, insulinimbalance, and endotoxemia—are theprimary causes oflaminitispathogenesis. Main Body. The Role of Metabolic Factors in the Development of Laminitis. Laminitis is a polyetiological disease occurring in cattle that primarily damages the connective structures between the hoof wall and the lamellar tissues. In imported high-yield dairy cows, this disease typically develops due to high productivity demands, inability to adapt to changes in the diet, and drastic differences in the rearing environment. Several key metabolic factors play a significant role in the pathogenesis of laminitis: Subacute Ruminal Acidosis (SARA). Imported breeds such as Holstein, Montbéliarde, and other high-producing cattle require a high-energy, balanced, and gradually adjustable diet. However, under Uzbekistan’s conditions, these animals are often fed with local energy feeds such as barley, wheat bran, silage, and molasses. Since the rumen microflora is not adapted to such rapidly fermentable feeds, the ruminal pH drops below 5.5, resulting in subacute ruminal acidosis (SARA). Under SARA conditions, lipopolysaccharides (LPS) released from the lysis of gram- negative bacteria translocate from the gut wall into the bloodstream. These endotoxins trigger inflammatory responses in the body and particularly adversely affect the capillary blood vessels of the hoof. This leads to capillary spasms, microthrombosis, and hypoxia, culminating in ischemia, necrosis, and edema of the lamellar tissues. Prolonged SARA episodes manifest clinically as inflammation centers in the hooves, internal fissures, and separation between the hoof wall and lamellar tissues. SARA is regarded as the "silent cause" of laminitis and remains the basis for many subclinical and chronic hoof pathologies. Insulin and Glucose Imbalance. High-producing breeds require significant energy expenditure for milk synthesis, prompting the organism to activate endogenous mechanisms 98,7:ROTCAFTCAPMI .SECNEICSLACIDEM ,5202, enuJ,5emuloV gro.srehsilbupcimedaca.www to maintain glucose homeostasis. This often results in hyperinsulinemia — an elevated insulin level in the blood. Insulin hypersecretion disrupts the function of endothelial cells in the blood vessels of the hoof, increasing capillary permeability. Endothelial dysfunction leads to micro-edema, pain, and dystrophic changes in the lamellar structures. Furthermore, hyperinsulinemia enhances the release of inflammatory cytokines (such as interleukin-1 and TNF-alpha), promoting the emergence of subclinical inflammatory foci in the hoof. In other words, the imbalance between insulin and glucose disturbs trophic metabolism in the hoof and creates a background conducive to laminitis development. Endotoxemia. Changes in rumen flora and disruption of intestinal epithelial barriers allow pathogenic microbes and their toxins (e.g., LPS, histamine, ammonia) to enter the bloodstream, causing endotoxemia. The LPS endotoxin reaches the lamellar capillaries of the hoof via circulation, disrupting microcirculation, inducing vascular spasms, and causing necrotic changes. Additionally, endocrine responses (such as cortisol secretion) are involved in this process, leading to an increase in inflammatory mediators and structural tissue chang