Oxytocin and cholecystokinin secretion in women with colectomy

BACKGROUND: Cholecystokinin (CCK) concentrations in plasma have been shown to be significantly higher in colectomised subjects compared to healthy controls. This has been ascribed to reduced inhibition of CCK release from colon. In an earlier study CCK in all but one woman who was colectomised, induced release of oxytocin, a peptide present throughout the gastrointestinal (GI) tract. The aim of this study was thus to examine if colectomised women had a different oxytocin response to CCK compared to healthy controls. METHODS: Eleven women, mean age 34.4 ± 2.3 years, who had undergone colectomy because of ulcerative colitis or constipation were studied. Eleven age-matched healthy women served as controls. All subjects were fasted overnight and given 0.2 μg/kg body weight of CCK-8 i.v. in the morning. Samples were taken ten minutes and immediately before the injection, and 10, 20, 30, 45, 60, 90 and 120 min afterwards. Plasma was collected for measurement of CCK and oxytocin concentrations. RESULTS: The basal oxytocin and CCK concentrations in plasma were similar in the two groups. Intravenous injection of CCK increased the release of oxytocin from 1.31 ± 0.12 and 1.64 ± 0.19 pmol/l to 2.82 ± 0.35 and 3.26 ± 0.50 pmol/l in controls and colectomised women, respectively (p < 0.001). Given the short half-life of CCK-8 in plasma, the increased concentration following injection could not be demonstrated in the controls. On the other hand, in colectomised women, an increase of CCK in plasma was observed for up to 20 minutes after the injection, concentrations increasing from 1.00 ± 0.21 to a maximum of 1.81 ± 0.26 pmol/l (p < 0.002). CONCLUSION: CCK stimulates the release of oxytocin in women. There is no difference in plasma concentrations between colectomised and controls. However, colectomy seems to reduce the metabolic clearance of CCK. The hyperCCKemia in patients who had undergone colectomy is consequently not only dependent on CCK release, but may also depend on reduced clearance

Pharmacometabolomics of Response to Sertraline and to Placebo in Major Depressive Disorder - Possible Role for Methoxyindole Pathway

10.1371/journal.pone.0068283PLoS ONE87-POLN

Nutritional Pearls: Diet and Rheumatoid Arthritis

Various studies have investigated the effect of diet on rheumatoid arthritis (RA) as a complimentary treatment along with standard drug therapy. Various types of diet have been investigated. Fasting, the Mediterranean diet, the Cretan Mediterranean diet, vegetarian diet, an anti-inflammatory diet and the use of various specific food substances have been in the focus of research interest. The relationship of obesity with disease activity in RA has also been investigated. A period of fasting followed by Mediterranean diet, the Cretan Mediterranean diet and an anti-inflammatory diet have been found to have a beneficial effect on disease activity in RA. Obesity has been found to be associated with increased disease activity in RA. However, weight loss appears to be related to increased mortality in RA. The use of flavonoids, resveratrol and curcumin may have a beneficial effect in RA. It appears that diet may aid in RA management as a complimentary factor to standard drug treatment. © 202

Vitamin D Deficiency in Primary Sjögren’s Syndrome: Association with Clinical Manifestations and Immune Activation Markers

Vitamin D is an agent involved in bone and mineral homeostasis. It has been recognized as a potent immunomodulator. It has immune-enhancing properties, and it induces immune tolerance. Vitamin D deficiency has been shown to be related to the development of autoimmune disorders. Vitamin D deficiency has been observed in patients with rheumatoid arthritis (RA) and it has been shown to be related with disease activity. Vitamin D deficiency has also been found in patients with systemic lupus erythematosus (SLE) and it was shown to be related to disease activity and renal involvement. Vitamin D deficiency has also been observed in multiple sclerosis. Vitamin D has been found to act as a supplemental therapeutic agent in multiple sclerosis. Sjögren’s syndrome is a systemic autoimmune disease affecting the exocrine glands, known as an autoimmune epithelitis. The disease has a complex pathogenesis, requiring a genetic background, immune cell activation, and autoantibody production. The disease affects the exocrine glands, lacrimal, and salivary glands leading to ocular and oral dryness. Vitamin D levels have been measured in patients with Sjögren’s syndrome and an association was observed between low vitamin D levels, peripheral neuropathy and the presence of lymphoma. In other cohorts, such as a Turkish cohort, vitamin D deficiency was observed in patients with Sjögren’s syndrome. The aim is to measure serum vitamin D levels in consecutive patients with primary Sjögren’s syndrome and investigate the relationship between vitamin D levels and the presence of immunologic markers, clinical, serological, and histopathological characteristics. © This work is licensed under a Creative Commons Attribution 4.0 International License

Vitamin D in acutely ill patients

Objective: To investigate 25(OH)D3 levels and their relationship to survival in a cohort of acutely ill patients on admission to an intensive care unit. Methods: This study enrolled acutely ill patients at admission to an intensive care unit and a group of sex- and age-matched healthy control subjects. The 25(OH)D3 levels were measured using an enzyme immunoassay. C-reactive protein and procalcitonin levels were also measured using immunoassays. Results: A total of 50 acutely ill patients and 50 healthy control subjects were enrolled in the study. The mean ± SEM 25(OH)D3 levels were significantly lower in the acutely ill patients compared with the control group (11.74 ± 0.88 ng/ml versus 24.66 ± 1.60 ng/ml, respectively). The 25(OH)D3 levels were not related to survival. An inverse relationship was observed between 25(OH)D3 levels and C-reactive protein levels. A weak inverse relationship was also observed between 25(OH)D3 levels and procalcitonin levels. Conclusions: The 25(OH)D3 levels were decreased in acutely ill patients admitted to an intensive care unit compared with healthy control subjects. 25(OH)D3 levels may be inversely related to C-reactive protein and procalcitonin levels. © The Author(s) 2018

Oxytocin release is inhibited by the generation of carbon monoxide from the rat hypothalamus--further evidence for carbon monoxide as a neuromodulator.

Recent evidence suggests that the gas nitric oxide can modulate the secretion of a number of hypothalamic hormones, and may be co-localized particularly to oxytocin-containing neurons. Another gas, carbon monoxide (CO), has also been suggested to play a role in neural signaling in the brain, and the synthetic enzyme responsible for the generation of carbon monoxide has been reported to be present in the rat hypothalamus. In this study, we have therefore investigated whether CO has the ability to modify the release of oxytocin from acute rat hypothalamic explants. Hemin, a specific CO precursor through the enzyme heme oxygenase (the enzymatic pathway synthesizing endogenous CO, was found to inhibit KCl-stimulated oxytocin release, with a maximal effect at 10(-5) M, while showing no effect on basal oxytocin secretion. The stimulation of oxytocin by serotonin 10 ng/ml was also significantly antagonized by hemin 10(-7) M. An inhibitor of heme oxygenase, zinc-protoporphyrin-9, had no effect on basal or stimulated oxytocin release. When hemin and zinc-protoporphyrin-9 were given together, the hemin-induced inhibition of oxytocin was completely antagonized by the enzyme inhibitor. Ferrous hemoglobin A0, a substance known to bind CO with high affinity, had no effect on either basal or stimulated oxytocin release, but when hemin and ferrous hemoglobin A0 were given together the hemin-induced inhibition of oxytocin was completely blocked. These findings provide evidence that endogenous CO may play a role in the control of oxytocin release and that, by analogy with nitric oxide, CO may represent a major new neuroendocrine modulator