The olfactory marker protein (OMP), which is also expressed in nonolfactory tissues, plays a role in regulating the kinetics and termination of olfactory transduction. Thus, we hypothesized that OMP may play a similar role in modulating the secretion of hormones involved in Ca2+ and cAMP signaling, such as glucagon. In the present study, we confirmed nonolfactory α-cell-specific OMP expression in human and mouse pancreatic islets as well as in the murine α-cell line αTC1.9. Glucagon and OMP expression increased under hyperglycemic conditions. Omp knockdown in hyperglycemic αTC1.9 cells using small-interfering RNA (siRNA) reduced the responses to glucagon release and the related signaling pathways compared with the si-negative control. The OMPlox/lox;GCGcre/w mice expressed basal glucagon levels similar to those in the wild-type OMPlox/lox mice but showed resistance against streptozotocin-induced hyperglycemia. The ectopic olfactory signaling events in pancreatic α-cells suggest that olfactory receptor pathways could be therapeutic targets for reducing excessive glucagon levels.

Aims: To Explore the role of apoptosis in pathogenesis and clinical manifestations of hashimoto thyroiditis (HT) through studying the relationship between peripheral blood concentration of apoptosis factors and thyroid function and related antibodies. Methods: Overall, we recruited 120 cases, including 90 female HT patients who are newly diagnosed and had not accepted any treatment and another 30 healthy controls. The exclusion criteria were current diagnosis or history of severe infections, diabetes, kidney disease and cardiovascular disease, and other autoimmune diseases as well as regular use of any medication. All patients were divided into four groups according to the thyroid function: normal group (group A: n=30), subclinical hypothyroidism group (group B: n=30), hypothyroidism group (group C: n=30). In addition, 30 healthy controls (group D: n=30). Serum B cell lymphoma-2 (Bcl-2), Bcl-2-Associated X (Bax) and Cytochrome C levels were determined by ELISA. Results: The correlation analysis result of Bax levels among four groups was F = 73.56, P < 0.0001, and Bax level of group B was higher than group A and group D, group C higher than that of group B(P < 0.05); Bcl-2 difference was statistically significant, F = 46.01, P < 0.0001, and group C lower than that of group A and group B, group D was higher than group A and group B( P < 0.05); Cytc of four groups was statistically significant difference, F = 141.58, P < 0.0001, and no statistically significant difference between group A and group D. Bax was negatively correlated with FT3 and FT4(r=-0.7057,-0.7177), which was positively correlated with TSH(r=0.6659), all P < 0.05. Bcl-2 was positively correlated with FT3 and FT4(r=0.5496,0.5596), which was negatively correlated with TSH (r=-0.5423), all P < 0.05; Cytc was negatively correlated with FT3 and FT4(r=-0.7027, -0.7733), which was positively correlated with TSH (r=0.7348), all P < 0.05. Bax was positively correlated with TgAb and TPOAb (r=0.4197,0.3020), both P < 0.05; Bcl-2 was negatively correlated with TgAb and TPOAb (-0.4633, -0.4232), both P < 0.05; Cytc was positively correlated with TgAb and TPOAb(r= 0.5816,0.2132 ), both P < 0.05. Conclusion: Bax and Cytc are positively correlated with thyroid antibody and hypothyroidism in HT patients, while Bcl-2 is negatively correlated with thyroid antibody and hypothyroidism in HT patients. Thus, apoptosis may be a thyroid function related pathogenesis of HT.