Search Results
Abstract
Objective—To determine cellular immunolocalization of canine gastric lipase (cGL) and canine pancreatic lipase (cPL) in various tissues obtained from clinically healthy dogs.
Sample Population—Samples of 38 tissues collected from 2 climically healthy dogs.
Procedures—The cGL and cPL were purified from gastric and pancreatic tissue, respectively, obtained from dogs. Antisera against both proteins were developed, using rabbits, and polyclonal antibodies were purified by use of affinity chromatography. Various tissues were collected from 2 healthy dogs. Primary antibodies were used to evaluate histologic specificity. Replicate sections from the collected tissues were immunolabeled for cGL and cPL and examined by use of light microscopy.
Results—Mucous neck cells and mucous pit cells of gastric glands had positive labeling for cGL, whereas other tissues did not immunoreact with cGL. Pancreatic acinar cells had positive labeling for cPL, whereas other tissues did not immunoreact with cPL.
Conclusions and Clinical Relevance—We concluded that cGL and cPL are exclusively expressed in gastric glands and pancreatic acinar cells, respectively. Also, evidence for cross-immunoreactivity with other lipases or related proteins expressed by other tissues was not found for either protein. Analysis of these data suggests that gastric lipase is a specific marker for gastric glands and that pancreatic lipase is a specific marker for pancreatic acinar cells. These markers may have clinical use in the diagnosis of gastric and exocrine pancreatic disorders, respectively. (Am J Vet Res 2002;63:722–727).
Abstract
OBJECTIVE
(1) Determine if a relationship exists between ionized calcium (iCa) and pancreatic lipase (cPLI) concentration in dogs, and (2) assess for correlation between resolving hypercalcemia and cPLI concentrations in dogs after treatment for primary hyperparathyroidism (PHPT).
SAMPLES
Phase I, 44 residual serum samples (collected April 2023) from client-owned dogs with a clinical indication for cPLI quantification. Phase II, 24 residual serum samples (collected August 2022 through February 2023) from client-owned dogs with PHPT pre- and postcorrection of hypercalcemia.
METHODS
Serum cPLI and iCa concentrations were measured via the Spec cPL assay and a spectrophotometric method respectively. Spearman’s rank correlation coefficients were used to investigate if there was a correlation between serum calcium and cPLI concentrations. A paired t-test was used to investigate the effect of the resolution of hypercalcemia on serum cPLI concentrations.
RESULTS
Phase I, serum cPLI concentrations were negatively correlated with serum iCa concentrations (r = −.429, 95% CI [−.64, −.14], P = .005) in dogs with a clinical indication for cPLI quantification. Phase II, median serum cPLI concentrations were higher before (median: 228.5 μg/L, IQR: 351.3 μg/L) than after (median: 141.0 μg/L, interquartile ranges (IQR): 279.5 μg/L) management of hypercalcemia (PHPT model). However, the decrease in cPLI concentration was not statistically significant (P = .70).
CLINICAL RELEVANCE
Calcium depletion may result in an inverse relationship between serum cPLI and iCa concentrations in dogs with a clinical indication for cPLI quantification. Hypercalcemia may be associated with an above reference interval cPLI concentration in some dogs.
not amenable to complete resection; however, a biopsy sample (approx 1 X 1 X 1 cm) was obtained. Histopathologic diagnosis of the mass was pancreatic acinar cell cystadenoma. Because resection was not a viable option, ongoing patient monitoring every
AP at hospital admission (ie, > 400 µg/L). Serum concentrations of cPL may not have any relation to the magnitude of either pancreatic impairment or AUS findings because serum cPL concentration only reflects pancreatic acinar cell injury. 12 In
. 23 Immunohistochemistry has demonstrated that pancreatic lipase is found exclusively in zymogen granules of pancreatic acinar cells and is thus pancreatic specific. 24 Pancreatic lipase and its cofactor, colipase, together with other pancreatic
. Clinical procedures . In: Biology and medicine of rabbits and rodents . 5th ed. Ames, Iowa : Wiley-Blackwell , 2007 ; 128 – 129 . 2. Sigler RE Gough AW Iglesia FA . Pancreatic acinar cell neoplasia in male Wistar rats following 2 years of
dogs and cats, including PAA, CP, pancreatic duct obstruction, and pancreatic neoplasia. In dogs, PAA is considered the most common cause of EPI. PAA is characterized by selective destruction of pancreatic acinar cells and their replacement with adipose
reliable indicator of disease severity. 4 , 13 , 25 , 26 Pancreatic lipase is released into the systemic circulation within minutes of damage to pancreatic acinar cells but has a short half-life (approx 2 hours). 27 If the trigger for pancreatic
The human SPINK1 gene encodes for a protein with a molecular mass of 6.5 kDa. This protein, pancreatic secretory typsin inhibitor, is produced, stored, and secreted by pancreatic acinar cells. 1 The gene has a length of approximately 7
catalytic assays, such as those used to measure lipase activity in serum. Recently, a new assay for measurement of PLI was developed and validated. 9 An immunolocalization study 10 revealed that only pancreatic acinar cells stain for pancreatic lipase
