Evaluation of the relationship between chronotype and biochemical findings, nutrition and gastrointestinal symptoms in inflammatory bowel patients.

This study was conducted with 39 inpatients diagnosed with IBD in the gastroenterology department of Samsun Ondokuz Mayis University Health Application and Research Center to evaluate the relationship between chronotype and biochemical findings, nutrition, and gastrointestinal symptoms in patients with inflammatory bowel disease. The data were collected using a general information form, Food Frequency Questionnaire, Gastrointestinal Symptom Rating Scale, and Morning-Evening Questionnaire. The biochemical findings of the patients were obtained from the medical records. Statistical analysis of the patients included in the study was performed with the SPSS package program. For all analyses, p < 0.05 was considered statistically significant. Twenty-eight patients were diagnosed with ulcerative colitis and 11 with Crohn's disease. There was a significant relationship between chronotype and daily polyunsaturated fatty acid and vitamin B6 intake in female subjects (p < 0.05). There was also a significant relationship between chronotype and percentage of carbohydrate consumed, polyunsaturated and saturated fatty acid intake in male subjects (p < 0.05). A significant relationship was found between chronotype and serum glucose, hematocrit, magnesium, and iron levels (p < 0.05). It was determined that while E-type had higher glucose and magnesium levels; M-type had higher hematocrit and iron levels. It was observed that there was a relationship between chronotype and biochemical findings and nutrition in patients with IBD. Chronotype is easy to determine and these results show that it should be considered as a factor when evaluating nutrition and clinical status in patients with IBD.

PDGF-ß receptor and PKC have no effect on angiotensin II-induced JAK2 and STAT1 phosphorylation in vascular smooth muscle cells under high glucose condition.

BACKGROUND: The mechanisms responsible for the accelerated cardiovascular disease in diabetes, as well as the increased hypertrophic effects of angiotensin II (Ang II) under hyperglycemic condition, are not very clear. Evidences show that platelet-derived growth factor (PDGF) and protein kinase C (PKC) play a critical role in this effect. In our study, we examined the role of PKC and PDGF receptor on JAK2 and STAT1 phosphorylation under high glucose (HG) condition (25 mmol/L) in response to Ang II in cultured vascular smooth muscle cells (VSMC). METHODS: VSMCs were isolated from the thoracic aorta of male Wistar rats and were cultured. Growth-arrested VSMCs were placed in either normal glucose (NG) or HG condition for 48 h and then VSMCs were stimulated with agonists and antagonists. The tyrosine phosphorylation of JAK2 or STAT were determined by immunoblotting using specific antibodies. RESULTS: High glucose markedly increased the phosphorylation of tyrosine residues of JAK2 and serine residues of STAT 1 compared with cells cultured in NG (5.5 mmol/L) with and without Ang II stimulation. Experiments made with specific PDGF-ß receptor inhibitor AG1295 and PKC inhibitor GF109203X showed that there were no changes in Ang II-stimulated JAK2 and STAT1 phosphorylation under NG and HG conditions compared with experiments without inhibitors. CONCLUSION: According to our findings, Ang II-stimulated JAK2 and STAT1 phosphorylation under either NG or HG condition do not proceed via a different pathway rather than PKC and PDGF-ß receptor.

Angiotensin II-induced MAPK phosphorylation mediated by Ras and/or phospholipase C-dependent phosphorylations but not by protein kinase C phosphorylation in cultured rat vascular smooth muscle cells.

Angiotensin II (Ang II) induces a rapid increase in mitogen-activated protein kinase (MAPK) activity through the Ang II type 1 receptor in cultured rat vascular smooth muscle cells (VSMCs). In the present study, we examined the effects of the phospholipase C (PLC) inhibitor U73122, the protein kinase C (PKC) inhibitor GF109203X, and the Ras inhibitor farnesylthiosalicylic acid (FTS) on Ang II-induced activation of p42/p44 MAPKs in cultured VSMCs. Phosphorylation was shown using the Western blot technique with specific phospho-antibodies against MAPK proteins. The PLC inhibitor U73122 abolished the Ang II-induced MAPK activity, while the PKC inhibitor GF109203X only decreased it. There was also an inhibition observed with the Ras inhibitor, FTS on Ang II-induced MAPK activity. These data suggest that Ang II-induced MAPK phosphorylation through the Ang II type 1 receptor could be mediated by Ras and/or PLC-dependent phosphorylations but not by PKC phosphorylation.