Involvement of apoptosis and proliferation of acinar cells in atrophy of rat parotid glands induced by liquid diet

Abstract

Parotid glands of experimental animals fed a liquid diet are reported to show atrophy (Hall and Schneyer 1964;Wilborn and Schneyer 1970;Hand and Ho 1981;Scott et al. 1990;Scott and Gunn 1991). To clarify whether apoptosis and proliferation of acinar cells participate in atrophy of rat parotid glands induced by liquid diet, rats were fed a liquid diet and compared to pellet-fed controls. Parotid glands were removed at 3, 7, 14 or 21 days, weighed, and examined using transmission electron microscopy (TEM), and studied immunohistochemically for cleaved-caspase-3 (Casp-3), a marker of apoptotic cells, and 5-bromo-2`-deoxyuridine (BrdU), a marker for proliferating cells. Body weights of experimental rats fed liquid diets were not significantly different from controls fed pellet diets; however weights of experimental parotid glands were smaller than those of controls. In the experimental parotid glands, structures like apoptotic bodies were histologically observed in acini at each time point; more Casp-3-positive acinar cells were identified in experimental parotid glands than in the controls on days 3, 7, and 14. Experimental glands showed fewer BrdU-positive acinar cells at each time point. TEM confirmed typical apoptotic acinar cells in the atrophic glands. These findings suggest that increased acinar cell apoptosis and reduced acinar cell proliferation occur in atrophic parotid glands of rats fed a liquid diet.

Immunohistochemical and ultrastructural investigation of acinar cells in submandibular and sublingual glands of rats fed a liquid diet

“…We demonstrated that a liquid diet did not induce atrophy in submandibular and sublingual glands, although parotid glands became atrophic under the same experimental conditions (Takahashi et al, 2012). This agreed with previous findings in submandibular (Ekstrom, 1973;Mansson et al, 1990;Kurahashi and Inomata, 1999) and sublingual glands (Ekstrom, 1973;Scott and Gunn, 1991) in studies using the same experimental conditions.…”

“…Previous studies suggested that changes in tissues of animals fed a liquid diet were not caused by changes in general health, because body weight loss or a general deterioration in health was not observed (Hall and Schneyer, 1964;Johnson, 1982;Mansson et al, 1990;Scott et al, 1990;Kurahashi and Inomata, 1999;Takahashi et al, 2012). In the present study, the body weights of experimental rats increased constantly and were not significantly different from those of controls, confirming the findings of previous studies.…”

“…Recently, we also 4 demonstrated increased apoptosis and reduced proliferative activity of acinar cells in parotid glands of rats fed a liquid diet (Takahashi et al, 2012). However, no studies have investigated apoptosis and proliferation of acinar cells in the submandibular and sublingual glands of liquid-fed rats.…”

“…To investigate these influences, an experimental model of feeding a liquid diet to animals is widely used. Parotid glands from liquid-fed animals become atrophic, acinar cells are reduced in size (Hand and Schneyer, 1964;Wilborn and Schneyer, 1970;Hand and Ho, 1981;Scott and Gunn, 1991;Takahashi et al, 2012) and acinar cell numbers decrease in the atrophic parotid glands (Johnson, 1982;Scott et al, 1990;Takahashi et al, 2012). Despite an increasing accumulation of knowledge regarding parotid glands of liquid-fed animals, few reports have investigated other salivary glands such as the submandibular and sublingual glands.…”

The Use of Electrophoresis for the Study of Saliva Involvement in Ingestive Behavior

“…Moreover, the physical and chemical properties of foods affect salivary glands morphology and histology [126][127][128][129]. Although the regulation of the secretory activity of salivary glands has been almost exclusively attributed to the autonomic nervous system [130], recent evidences suggest that during variations in appetite and food intake the glands are probably also regulated by gastric (gastrin) and intestinal (cholecystokinin and melatonin) hormones [131][132][133].…”