ALTERATION OF TASTE BUDS IN EXPERIMENTAL CIRRHOSIS. Is there correlation with human hypogeusia?

Abstract

-Background -The inherent complications of cirrhosis include protein-calorie malnutrition and micronutrient deficiencies.Changes in taste are detrimental to the nutritional status, and the mechanism to explain these changes is not well documented in the cirrhotic patients. Objective -To evaluate the taste buds of cirrhotic rats. Methods -Fourteen male Wistar rats were evaluated. After 16 weeks, the liver was removed to histologically diagnose cirrhosis, and blood was collected to perform liver integrity tests. The tongue was removed for histological examination and immunohistochemistry using antibodies against protein gene product PGP 9.5 and the sweet taste receptors T1R2 and T1R3. Morphological changes were determined by scanning electron microscopy. Serum zinc levels were measured. Results -The cirrhotic animals, but not the control animals, exhibited zinc deficiency. In both groups, there was positive immunoreactivity for type II and III cells and T1R2 receptors. The cirrhotic animals had no immunoreactivity for T1R3 receptors. Scanning electron microscopy analysis of the cirrhotic group revealed a uniform tapering of the gustatory papillae. Conclusion -In conclusion the experimental cirrhosis model mimicked the biochemical and histological parameters of human cirrhosis, therefore enabling a study of the gustatory papillae and taste buds.

Melatonin restores zinc levels, activates the Keap1/Nrf2 pathway, and modulates endoplasmic reticular stress and HSP in rats with chronic hepatotoxicity

“…As already observed in the study by Fernandes et al [ 59 ], cirrhotic animals showed significantly lower serum levels of zinc when compared to controls, showing an association of zinc deficiency with liver damage in sick animals.…”

“…Studies linking zinc and liver diseases often described that the replacement of the zinc element results in an improvement in the clinical and morphological condition[ 7 , 59 ]. We determined the zinc levels in the liver of rats exposed to CCl 4 .…”

Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis

“…Hypozincemia, or zinc deficiency in liver disease, is associated with the development of alterations in taste and smell as well as anorexia, which can further contribute to a decreased food intake as well as increased gastrointestinal and urinary losses [ 23 ]. In patients with liver cirrhosis, the two most common symptoms related to taste are sweet taste aversion and salty taste intolerance, but also a metallic taste is frequently observed [ 79 ], whereby patients with hypozincemia report having either a dry mouth or a metallic taste [ 23 ]. The urinary loss of zinc is aggravated by the prevalent use of diuretics used to treat edema and ascites [ 80 ].…”

Factors Associated Towards Malnutrition in Liver Cirrhosis Patient: A Literature Review

“…The pathophysiology of malnutrition in cirrhosis is heavily influenced by the fact that many individuals with the disease have decreased dietary intake (15). A comprehensive understanding of the factors contributing to a negative energy balance, such as inflammation, early satiety from ascites, hepatic encephalopathy, negative gastrointestinal symptoms, taste alterations, and unappealing dietary restrictions, is necessary in identifying effective therapies to increase food intake (16)(17)(18). However, it still needs to be determined which of these elements contributes an essential role.…”