GMT has been described in debilitated rodents and in general is associated with cachexia (e.g., secondary to neoplasia, endocrinopathies) and advanced severe malnutrition (e.g., maldigestion). Under current husbandry standards, however, GMT is rarely encountered in NTP studies today. Although the pathogenesis of GMT remains unclear, its association with a wide range of diseases suggests it may result from basic bioregulatory processes that are activated in states of advanced illness. It has been suggested that the ground substance may be a replacement for the adipocytes that are used in catabolic states of disease, while the hematopoietic cell loss may be due to an unfavorable bone marrow microenvironment related to inadequate hematopoietic substrates and lack of stimulation by adipocytes and fibrocytes.
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