Soluble CD40 Ligand Levels in Otherwise Healthy Subjects With Impaired Fasting Glucose

Unlike diabetes mellitus and impaired glucose tolerance, it is not clear whether the subjects with impaired fasting glucose (IFG) are at increased risk of atherosclerosis and cardiovascular diseases. The CD40-CD40 ligand interaction is involved in the mechanism of atherosclerosis. We investigated whether soluble CD40L (sCD40L) as well as high sensitive C-reactive protein (hsCRP) levels are increased in subjects with IFG having no confounding factors for inflammation or atherosclerosis. Twenty four IFG subjects with no additional disorders and 40 appropriate healthy controls were studied. sCD40L and hsCRP levels in the IFG and control groups were similar. Blood pressures, total and LDL-cholesterol, and triglyceride levels were also similar, whereas HDL-cholesterol was lower and HOMA-IR indexes were higher in the IFG group. Though the sample size was small, the present data show that sCD40L seems not to alter in subjects with IFG suggesting that it might not be an independent risk factor for atherosclerosis

Protein losing enteropathy: A rare complication of ulcerative colitis

Protein-losing enteropathy (PLE) is a rare gastrointestinal condition that has been related to inflammatory bowel disease (IBD), namely ulcerative colitis (UC) and Crohns disease (CD). These pathologies damage the mucosal integrity, thereby leading to an increased transfer of plasma proteins into the bowel lumen. Because of its rarity, incidence and prevalence of this condition are not well known. Depending upon the underlying cause, the clinical course of PLE is highly variable, but mainly consists of edema, ascites, pericardial and pleural effusions. Here, we report a case of PLE caused by UC, in which total colectomy lead to complete improvement of hypoalbuminemia. [Med-Science 2019; 8(4.000): 1041-3

The Evolving Role of Fetuin-A in Nonalcoholic Fatty Liver Disease: An Overview from Liver to the Heart

Nonalcoholic fatty liver disease (NAFLD) is strongly associated to the features of metabolic syndrome which can progress to cirrhosis, liver failure and hepatocellular carcinoma. However, the most common cause of mortality in people with NAFLD is not liver-related but stems from atherosclerotic cardiovascular disease (CVD). The prevalence of NAFLD is on the rise, mainly as a consequence of its close association with two major worldwide epidemics, obesity and type 2 diabetes (T2D). The exact pathogenesis of NAFLD and especially the mechanisms leading to disease progression and CVD have not been completely elucidated. Human fetuin-A (alpha-2-Heremans Schmid glycoprotein), a glycoprotein produced by the liver and abundantly secreted into the circulation appears to play a role in insulin resistance, metabolic syndrome and inflammation. This review discusses the links between NAFLD and CVD by specifically focusing on fetuin-A’s function in the pathogenesis of NAFLD and atherosclerotic CVD

Transforming growth factor beta (TGF-beta) levels in otherwise healthy subjects with impaired glucose tolerance

KISA, Ucler/0000-0002-8131-6810; Naharci, Mehmet/0000-0003-2730-7144; GENC, HALIL/0000-0002-0229-1695; Sonmez, Alper/0000-0002-9309-7715WOS: 000208625900008PubMed: 21104643Introduction: Serum transforming growth factor beta (TGF-beta) level is increased in type-2 diabetes mellitus (T2DM) and certain diabetic complications are mediated by this cytokine. Impaired glucose tolerance (IGT) is a prediabetic condition, and confers a risk for the development of certain diabetes-specific complications. However, no data is available regarding the alteration of TGF-beta in IGT subjects. Therefore, we aimed to investigate TGF-beta levels in otherwise healthy subjects with IGT. Material and methods: Thirty IGT subjects and 30 subjects relatively matched for age, sex and body mass index with normal glucose tolerance were enrolled. Subjects with overt diabetes, cardiovascular, renal or inflammatory disease, or on any medication were excluded. Relevant laboratory examinations were performed by routine methods. Assessment of TGF-beta was made by a commercially available enzyme-linked immunosorbent assay kit. IGT and control subjects were compared for their clinical and laboratory parameters. Results: Serum TGF-beta levels were found to be similar in IGT and normal glucose tolerance subjects (p < 0.05). No statistically significant correlation was found between TGF-beta and other laboratory parameters, either in IGT subjects or in the whole study population. Conclusions: Serum TGF-beta is not elevated in otherwise healthy subjects with IGT. The results of our study imply that the presence of IGT alone is not sufficient to induce TGF-beta elevation; and for the alteration of TGF-beta, worsening of metabolic risk factors may be required. (Pol J Endocrinol 2010; 61 (6): 691-694)Gulhane MilitaryMedical AcademyThis study is financially supported by grants from Gulhane MilitaryMedical Academy. There is no conflict of interest

Transforming growth factor &#946; (TGF-&#946;) levels in otherwise healthy subjects with impaired glucose tolerance

Wstęp: U chorych na cukrzycę typu 2 zwiększa się stężenie transformującego czynnika wzrostu beta (TGF-&#946;, transforming growth factor beta). Cytokina ta pośredniczy w rozwoju wielu powikłań cukrzycowych. Nieprawidłową tolerancję glukozy (IGT, impaired glucose tolerance) uważa się za stan przedcukrzycowy. Zaburzenie to wiąże się ze zwiększonym ryzykiem niektórych powikłań charakterystycznych dla cukrzycy. Brakuje danych dotyczących zmian stężenia TGF-&#946; u osób z IGT. Dlatego też autorzy postanowili zbadać osoczowe stężenia tego czynnika u zdrowych osób z IGT. Materiał i metody: Do badania włączono 30 osób z IGT i 30 osób z prawidłową tolerancją glukozy dobranych pod względem wieku, płci i wskaźnika masy ciała. Kryteria wykluczenia obejmowały jawną cukrzycę, choroby sercowo-naczyniowe, choroby nerek i choroby zapalne oraz przyjmowanie jakichkolwiek leków. Odpowiednie badania laboratoryjne przeprowadzono rutynowymi metodami. Stężenia TGF-&#946; zmierzono, stosując komercyjny zestaw immunoenzymatyczny. Porównano parametry kliniczne i laboratoryjne w grupie osób z IGT i grupie kontrolnej. Wyniki: Osoczowe stężenia TGF-&#946; były podobne u osób z IGT i z prawidłową tolerancją glukozy (p < 0,05). Nie stwierdzono istotnych statystycznie korelacji pomiędzy stężeniem TGF-&#946; i innymi parametrami laboratoryjnymi ani w grupie osób z IGT, ani w całej badanej populacji. Wnioski: U zdrowych osób z IGT stężenie TGF-&#946; w osoczu nie było podwyższone. Wyniki przeprowadzonego przez autorów badania wskazują, że do wywołania zmian stężenia TGF-&#946; nie wystarcza sama IGT, lecz konieczne jest współwystępowanie innych metabolicznych czynników ryzyka. (Endokrynol Pol 2010; 61 (6): 691-694)Introduction: Serum transforming growth factor beta (TGF-&#946;) level is increased in type-2 diabetes mellitus (T2DM) and certain diabetic complications are mediated by this cytokine. Impaired glucose tolerance (IGT) is a prediabetic condition, and confers a risk for the development of certain diabetes-specific complications. However, no data is available regarding the alteration of TGF-&#946; in IGT subjects. Therefore, we aimed to investigate TGF-&#946; levels in otherwise healthy subjects with IGT. Material and methods: Thirty IGT subjects and 30 subjects relatively matched for age, sex and body mass index with normal glucose tolerance were enrolled. Subjects with overt diabetes, cardiovascular, renal or inflammatory disease, or on any medication were excluded. Relevant laboratory examinations were performed by routine methods. Assessment of TGF-&#946; was made by a commercially available enzyme-linked immunosorbent assay kit. IGT and control subjects were compared for their clinical and laboratory parameters. Results: Serum TGF-&#946; levels were found to be similar in IGT and normal glucose tolerance subjects (p < 0.05). No statistically significant correlation was found between TGF-&#946; and other laboratory parameters, either in IGT subjects or in the whole study population. Conclusions: Serum TGF-&#946; is not elevated in otherwise healthy subjects with IGT. The results of our study imply that the presence of IGT alone is not sufficient to induce TGF-&#946; elevation; and for the alteration of TGF-&#946;, worsening of metabolic risk factors may be required. (Pol J Endocrinol 2010; 61 (6): 691-694

Association of plasma visfatin with hepatic and systemic inflammation in nonalcoholic fatty liver disease

Background. Visfatin is a proinflammatory and insulin-mimetic adipokine contributing to whole body glucose and lipid metabolism. Studies to date are conflicting regarding the relationship between visfatin and non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to evaluate the relationship of circulating visfatin with NAFLD. Material and methods. The study included 114 NAFLD patients and 60 healthy non-diabetic controls. Plasma visfatin, adiponectin, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels were measured by ELISA. High sensitive C-reactive protein (hsCRP) levels were measured by immunoturbidimetric fixed rate method. Insulin sensitivity determined by homeostasis model assessment (HOMA-IR) index. Results. TNF-α, IL-6 and hsCRP levels were higher and, Adiponectin levels were lower in NAFLD group when compared to healthy controls (p < 0.001, for all). However, no difference was found regarding to visfatin levels between two groups. Different histologic subgroups of NAFLD had a significantly higher TNF-α, IL-6 and hsCRP, and lower adiponectin levels than those with controls (p < 0.001, for all). On the other hand, no statistically significant difference was found regarding to visfatin levels among different histologic groups. Visfatin was found to be negatively correlated with TNF-α (r = −0.236, p = 0.011) in NAFLD group. However, no association was found between visfatin and histological findings. Conclusion. Our findings show that plasma visfatin levels are not altered in the early stages of NAFLD. However, it is inversely associated with TNF-α. These findings suggest a role for visfatin in protection against liver injury in this widespread disease