Effects of Supplemental Mannanoligosaccharides on Growth Performance, Faecal Characteristics and Health in Dairy Calves

Kara, Cagdas,Cihan, Huseyin,Temizel, Mutlu,Catik, Serkan,Meral, Yavuz,Orman, Abdulkadir,Yibar, Artun,Gencoglu, Hidir Asian Australasian Association of Animal Productio 2015 Animal Bioscience Vol.28 No.11

Twenty Holstein calves were used to investigate the effects of mannanoligosaccharides (MOS) supplementation in the whole milk on growth performance, faecal score, faecal pH, selected faecal bacterial populations and health during the preweaning period. Healthy calves selected by clinical examination were allocated to one of the two groups (control [CG] and experimental [EG]) at 5 days old. Each group consisted of 5 male and 5 female calves. Each calf in EG was supplemented with 7 g/d of a MOS product (Celmanax) from 5 days to 56 days of age. MOS supplement was mixed with the whole milk once in the morning and administered to the calves in EG via nipple bottle, whereas the calves in CG were fed the whole milk without MOS. Calves were weaned at 56 days of age. The final body weight, average daily weight gain (ADG) and average daily feed intake (ADFI) were statistically similar (p>0.05) but were higher by 3.70%, 6.66%, and 10.97%, respectively, in MOS than in control calves. Feed efficiency (ADG/ADFI) was also similar in two calves group. While faecal scores did not differ on day 5, 7, 14, 21, 28, 42, 49, and 56 between groups, EG had a higher faecal score (p = 0.05) than CG on day 35. Faecal concentration of Lactobacillus was lower (p<0.05) in EG compared with CG. No differences (p>0.05) in faecal concentrations of Bifidobacterium, Clostridium perfringens, and Escherichia coli were found between groups. Although there were no significant differences (p>0.05) in the incidence of diarrhoea, treatment days for diarrhoea and the costs associated with diarrhoea treatments between groups, collectively, the observed reductions in treatment days and the cost of diarrhoea treatments accompanying increases in final body weight, ADG and ADFI for EG may indicate potential benefit of MOS in treatment of diarrhoea.

Serum Visfatin and Fetuin-A Levels and Glycemic Control in Patients with Obese Type 2 Diabetes Mellitus

Fethiye Oztop Gunduz,Sembol Turkmen Yildirmak,Mustafa Temizel,Yilmaz Faki,Mustafa Cakmak,Mustafa Durmuscan,Funda Sezgin 대한당뇨병학회 2011 Diabetes and Metabolism Journal Vol.35 No.5

Background: Visfatin is an adipokine produced by visceral adipose tissue and has insulin-mimicking effects. Fetuin-A is a hepatic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro. The authors of the present study aimed to investigate the levels of serum visfatin and fetuin-A and their correlation with hemoglobin A1c (HbA1c) and urine albumin levels in patients with type 2 diabetes mellitus (T2DM). Methods: A total of 40 obese patients with T2DM (11 males and 29 females; age, 54.47±10.83 years and 23 obese nondiabetic controls (8 males and 15 females; age, 53.04±11.33 years) were included in the study. Age, sex, and body mass index were similar in the 2 groups. Serum visfatin and fetuin-A levels were measured by enzyme-linked immunosorbent assay. HbA1c and urine albumin levels were measured by high performance liquid chromatography and nephelometric method, respectively. Results: Serum levels of visfatin in patients with T2DM (4.03±2.44 ng/mL) were similar to the control group (3.65±3.02 ng/mL). Serum fetuin-A levels were significantly lower in patients with T2DM than the controls (298.75±78.86 and 430.73±94.46 μg/mL, respectively). HbA1c levels were significantly higher in the T2DM group compared with controls (7.33±1.32 and 5.44±0.84%, respectively). Correlations between visfatin, fetuin-A and HbA1c levels were not observed. Conclusion: The present study suggests fetuin-A may play a role in the pathogenesis of T2DM.

Effects of Supplemental Mannanoligosaccharides on Growth Performance, Faecal Characteristics and Health in Dairy Calves

Cagdas Kara,Huseyin Cihan,Mutlu Temizel,Serkan Catik,Yavuz Meral,Abdulkadir Orman,Artun Yibar,Hidir Gencoglu 아세아·태평양축산학회 2015 Animal Bioscience Vol.28 No.11

Twenty Holstein calves were used to investigate the effects of mannanoligosaccharides (MOS) supplementation in the whole milk on growth performance, faecal score, faecal pH, selected faecal bacterial populations and health during the preweaning period. Healthy calves selected by clinical examination were allocated to one of the two groups (control [CG] and experimental [EG]) at 5 days old. Each group consisted of 5 male and 5 female calves. Each calf in EG was supplemented with 7 g/d of a MOS product (Celmanax) from 5 days to 56 days of age. MOS supplement was mixed with the whole milk once in the morning and administered to the calves in EG via nipple bottle, whereas the calves in CG were fed the whole milk without MOS. Calves were weaned at 56 days of age. The final body weight, average daily weight gain (ADG) and average daily feed intake (ADFI) were statistically similar (p>0.05) but were higher by 3.70%, 6.66%, and 10.97%, respectively, in MOS than in control calves. Feed efficiency (ADG/ADFI) was also similar in two calves group. While faecal scores did not differ on day 5, 7, 14, 21, 28, 42, 49, and 56 between groups, EG had a higher faecal score (p = 0.05) than CG on day 35. Faecal concentration of Lactobacillus was lower (p<0.05) in EG compared with CG. No differences (p>0.05) in faecal concentrations of Bifidobacterium, Clostridium perfringens, and Escherichia coli were found between groups. Although there were no significant differences (p>0.05) in the incidence of diarrhoea, treatment days for diarrhoea and the costs associated with diarrhoea treatments between groups, collectively, the observed reductions in treatment days and the cost of diarrhoea treatments accompanying increases in final body weight, ADG and ADFI for EG may indicate potential benefit of MOS in treatment of diarrhoea.

Homozygous Missense Epithelial Cell Adhesion Molecule Variant in a Patient with Congenital Tufting Enteropathy and Literature Review

Guvenoglu, Merve,Simsek-Kiper, Pelin Ozlem,Kosukcu, Can,Taskiran, Ekim Z.,Saltik-Temizel, Inci Nur,Gucer, Safak,Utine, Eda,Boduroglu, Koray The Korean Society of Pediatric Gastroenterology 2022 Pediatric gastroenterology, hepatology & nutrition Vol.25 No.6

Congenital diarrheal disorders (CDDs) with genetic etiology are uncommon hereditary intestinal diseases characterized by chronic, life-threatening, intractable watery diarrhea that starts in infancy. CDDs can be mechanistically divided into osmotic and secretory diarrhea. Congenital tufting enteropathy (CTE), also known as intestinal epithelial dysplasia, is a type of secretory CDD. CTE is a rare autosomal recessive enteropathy that presents with intractable neonatal-onset diarrhea, intestinal failure, severe malnutrition, and parenteral nutrition dependence. Villous atrophy of the intestinal epithelium, crypt hyperplasia, and irregularity of surface enterocytes are the specific pathological findings of CTE. The small intestine and occasionally the colonic mucosa include focal epithelial tufts. In 2008, Sivagnanam et al. discovered that mutations in the epithelial cell adhesion molecule (EpCAM, MIM# 185535) were the genetic cause of CTE (MIM# 613217). More than a hundred mutations have been reported to date. Furthermore, mutations in the serine peptidase inhibitor Kunitz type 2 (SPINT2, MIM# 605124) have been linked to syndromic CTE. In this study, we report the case of a 17-month-old male infant with congenital diarrhea. Despite extensive etiological workup, no etiology could be established before admission to our center. The patient died 15 hours after being admitted to our center in a metabolically decompensated state, probably due to a delay in admission and diagnosis. Molecular autopsy with exome sequencing revealed a previously reported homozygous missense variant, c.757G>A, in EpCAM, which was confirmed by histopathological examination.

Distinctive Features of Hepatic Steatosis in Children: Is It Primary or Secondary to Inborn Errors of Metabolism?

Karhan, Asuman Nur,Hizarcioglu-Gulsen, Hayriye,Gumus, Ersin,Akcoren, Zuhal,Demir, Hulya,Saltik-Temizel, Inci Nur,Orhan, Diclehan,Ozen, Hasan The Korean Society of Pediatric Gastroenterology 2021 Pediatric gastroenterology, hepatology & nutrition Vol.24 No.6

Purpose: The incidence of hepatic steatosis among children has been increasing; however, data distinguishing simple steatosis from a more complex disorder are lacking. Methods: This study identified the etiologies resulting in hepatic steatosis through a retrospective review of pediatric liver biopsies performed in the last 10 years. A total of 158 patients with hepatic steatosis proven by histopathological evaluation were enrolled in the study, and baseline demographic features, anthropometric measurements, physical examination findings, laboratory data, ultrasonographic findings, and liver histopathologies were noted. Results: The two most common diagnoses were inborn errors of metabolism (IEM) (52.5%) and nonalcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) (29.7%). The three most common diseases in the IEM group were glycogen storage disorders, Wilson's disease, and mitochondrial disease. The rates of consanguineous marriage (75.6%; odds ratio [OR], 26.040) and positive family history (26.5%; OR, 8.115) were significantly higher (p=0.002, p<0.001, respectively) in the IEM group than those in the NAFLD/NASH group. Younger age (p=0.001), normal anthropometric measurements (p=0.03), increased aspartate aminotransferase levels (p<0.001), triglyceride levels (p=0.001), and cholestatic biochemical parameters with disrupted liver function tests, as well as severe liver destruction of hepatic architecture, cholestasis, fibrosis, and nodule formation, were also common in the IEM group. Conclusion: Parents with consanguinity and positive family history, together with clinical and biochemical findings, may provide a high index of suspicion for IEM to distinguish primary steatosis from the consequence of a more complex disorder.