Effect of hesperidin treatment on α-Klotho/FGF-23 pathway in rats with experimentally-induced diabetes

Objective Non-alcoholic fatty liver disease, steatohepatitis and nephropathy are considered among the mostimportant complications of diabetes mellitus (DM), which recently increased due to increased frequency of DMand the prolonged life span of diabetic patients The aim of the present study was to reveal the possible effect ofhesperidin (HP) on alpha-klotho (α-KL)/fibroblast growth factor-23 (FGF-23) pathway in rats with diabetesinduced by streptozotocin (STZ).Materials and methods Thirty six male Sprague-Dawley rats were randomly divided into three groups. Therats of the control, diabetes, and treatment groups were fed with standard feed and water throughout the 2-weekstudy. In order to induce diabetes mellitus in rats, those in the diabetes group were administered a single dose of50 mg/kg STZ. For the DM + HP group, a single dose of 50 mg/kg STZ, when diabetes was induced, hesperidinwas administered orally at a dose of 100 mg/kg by gavage.Results Theα-KL levels of our study groups, both the liver and kidneyα-KL levels and serumα-KL of the STZ-induced diabetic group were statistically significantly lower than the control group (respectively, p < 0.05,p < 0.001, p < 0.05). It was observed that hesperidin administration statistically significantly increasedα-KLlevels in serum, liver and renal tissue (p < 0.001). Liver, kidney and serum FGF-23 levels of the diabetic groupincreased significantly in comparison to the control group (respectively, p < 0.05, p < 0.01, p < 0.001). FGF-23 levels that increased in kidney tissue and serum samples of the diabetic group decreased statistically sig-nificantly with hesperidin administration (respectively, p < 0.01, p < 0.001).Conclusion Theα-KL/FGF-23 pathway is a promising bio-indicator in various cases of systemic toxicity andpathology. In addition, the strong positive effects of hesperidin administration on diabetic toxicity in the liverand kidneys suggest that it may be included in the alternative treatment methods in the future.This work was supported by Coordinator of Scientific Research Projects ( 2017.M83.02.01 ) at University of Artvin Coruh

Our cases with familial hypocalciuric hypercalcemia

Ailesel hipokalsiürik hiperkalsemi, ılımlı hiperkalsemi, idrarda kalsiyum atılımının az olması ile giden ve kalsiyum duyarlı reseptörlerde mutasyonlardan kaynaklanan benign bir hastalıktır. 2010 Ocak ile 2015 Haziran ayları arasında İç hastalıkları polikliniğimize başvuran altı hasta klinik ve biyokimyasal parametrelerle değerlendirilmiştir. Olgularımız, 21 ile 86 yaş arasında, dördü kadın olmak üzere toplam altı hasta idi. Beş olgumuzun çocukları ve bir olgumuzun ebeveynleri poliklinik ortamında değerlendirildi. Olguların değerlendirmesinde ılımlı hiperkalsemi, sınırda yüksek parathormon düzeyleri ve idrarla günlük kalsiyum atılımının belirgin düşüklüğü nedeniyle ailesel hipokalsiürik hiperkalsemi olabileceği düşünüldü. Beş erişkin hastanın çocuklarında ve bir genç hastamızın da annesinde kalsiyum metabolizmasında benzer laboratuvar bulguları saptanması ve hiperkalsemi yapan diğer nedenlerin dışlanması üzerine tanı doğrulandı.Familial hypocalciuric hypercalcemia is a benign disease caused by mutations in the calcium-sensitive receptors, with moderate hypercalcemia and of calcium excretion in the urine leading to less. Six patients was evaluated in our internal medicine polyclinic with clinic and biochemistry parameters between 2010 January and 2015 June. Our cases were six patients including four women between 21 and 86 old. We evaluated in our polyclinic five cases childs and one cases parents. The results of evaluation of the patients were thought to be familial hypocalciuric hypercalcemia because of moderate hypercalcemia, borderline high parathormone levels and marked impairment of urinary calcium excretion. The diagnosis was confirme exclusion of other causes of hypercalcemia and the childrens of five patients and mother of one patients detected in calcium metabolism in the laboratory findings are similar to

Responses Of Anterior Pituitary Hormones To Fever During Community-Acquired Infections

Aim: The aim of the study was to determine the responses of adrenal corticotropic hormone (ACTH), cortisol, thyroid-stimulating hormone (TSH) and prolactin (PRL) levels during community-acquired infections with fever and to compare changes of these hormones to febrile and afebrile episodes. Methods: Plasma levels of ACTH, serum levels of cortisol, TSH and PRL of 60 hospitilized patients were evaluated prospectively. Blood samples from study group were taken 2 times; during pyrexia and one hour after decreasing of fever. Only one blood sample was taken from each control patient and time of blood sampling was same for all of them. Results: 60 hospitalized patients were included to the study. Of these, 29 were study group, 31 were control group. In febrile patients with infection; plasma ACTH levels was higher than the control group (37,35±35,82 pg/mL vs 22,78±28,84 pg/mL) but no statistical significance was found (p=0,101). Serum cortisol levels was higher than the control group (28,88±13,12 ug/dL vs 17,68±7,88 ug/dL) (p<0,001). There were no differences in serum PRL and TSH levels between the two groups. In the study group plasma ACTH and cortisol levels were significantly increased in febrile periods when compared to afebrile periods (32,21±28,51 pg/mL vs 18,93±22,86. pg/mL; p=0,002) and (28,32±12,96 ug/dL vs 23,09±15,05 ug/dL; p=0,024) respectively. In PRL and TSH levels there was no statistically significance. Conclusion: We concluded that plasma ACTH and serum cortisol elevations are common in acute infectious diseases, and they are more sensitive to increasing of body temperature. The two peptides may be involved in central mediation of fever, perhaps limiting the febrile response acting as neuromodulators in central thermoregulatory pathways