63 research outputs found
The Use of Proton Pump Inhibitors May Increase Symptoms of Muscle Function Loss in Patients with Chronic Illnesses
Long-term use of proton pump inhibitors (PPIs) is common in patients with muscle
wasting-related chronic diseases. We explored the hypothesis that the use of PPIs may contribute to
a reduction in muscle mass and function in these patients. Literature indicates that a PPI-induced
reduction in acidity of the gastrointestinal tract can decrease the absorption of, amongst others,
magnesium. Low levels of magnesium are associated with impaired muscle function. This
unwanted side-effect of PPIs on muscle function has been described in different disease backgrounds.
Furthermore, magnesium is necessary for activation of vitamin D. Low vitamin D and magnesium
levels together can lead to increased inflammation involved in muscle wasting. In addition, PPI use
has been described to alter the microbiotaâs composition in the gut, which might lead to increased
inflammation. However, PPIs are often provided together with nonsteroidal anti-inflammatory drugs
(NSAIDs), which are anti-inflammatory. In the presence of obesity, additional mechanisms could
further contribute to muscle alterations. In conclusion, use of PPIs has been reported to contribute to
muscle function loss. Whether this will add to the risk factor for development of muscle function loss
in patients with chronic disease needs further investigation
Differences in food intake of tumour-bearing cachectic mice are associated with hypothalamic serotonin signalling
A diet rich in fish oil and Leucine Ameliorates Hypercalcemia in tumour-induced cachectic mice
Background: Dietary supplementation with leucine and fish oil rich in omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) has previously been shown to reduce cachexia-related outcomes in C26 tumour-bearing mice. To further explore associated processes and mechanisms we investigated changes in plasma Ca2+ levels, the involvement of parathyroid hormone related protein (PTHrP), and its possible interactions with cyclooxygenase 2 (COX-2). Methods: CD2F1 mice were subcutaneously inoculated with C26 adenocarcinoma cells or sham treated and divided in: (1) controls, (2) tumour-bearing controls, and (3) tumour-bearing receiving experimental diets. After 20 days, body and organ masses and total plasma Ca2+ levels were determined. Furthermore, effects of DHA, EPA and leucine on production of PTHrP were studied in cultured C26 cells. Results: The combination of leucine and fish oil reduced tumour-associated hypercalcemia. Plasma Ca2+ levels negatively correlated with carcass mass and multiple organ masses. DHA was able to reduce PTHrP production by C26 cells in vitro. Results indicate that this effect occurred independently of COX-2 inhibition. Conclusion: Our results suggest that cancer-related hypercalcemia may be ameliorated by a nutritional intervention rich in leucine and fish oil. The effect of fish oil possibly relates to a DHA-induced reduction of PTHrP excretion by the tumour
A Logical Study of Distributed Transition Systems
AbstractWe extend labelled transition systems to distributed transition systems by labelling the transition relation with a finite set of actions, representing the fact that the actions occur as a concurrent step. We design an addition-based temporal logic in which one can explicity talk about steps. The logic is studied to establish a variety of positive and negative results in terms of axiomatizability and decidability. Our positive results show that the step notion is amenable to logical treatment via standard techniques. They also help us to obtain a logical characterization of two well known models for distributed systems: labelled elementary net systems and labelled prime event structures. Our negative results show that demanding deterministic structures when dealing with a "non-interleaved" notion of transitions is, from a logical standpoint, very expressive. They also show that another well known model of distributed systems called asynchronous transition systems exhibits a surprising amount of expressive power in a natural logical setting
Appetite Control across the Lifecourse: The Acute Impact of Breakfast Drink Quantity and Protein Content. The Full4Health Project
Understanding the mechanisms of hunger, satiety and how nutrients affect appetite control is important for successful weight management across the lifecourse. The primary aim of this study was to describe acute appetite control across the lifecourse, comparing age groups (children, adolescents, adults, elderly), weight categories, genders and European sites (Scotland and Greece). Participants (n = 391) consumed four test drinks, varying in composition (15% (normal protein, NP) and 30% (high protein, HP) of energy from protein) and quantity (based on 100% basal metabolic rate (BMR) and 140% BMR), on four separate days in a double-blind randomized controlled study. Ad libitum energy intake (EI), subjective appetite and biomarkers of appetite and metabolism (adults and elderly only) were measured. The adultsâ appetite was significantly greater than that of the elderly across all drink types (p 0.004) and in response to drink quantities (p 0.001). There were no significant differences in EI between age groups, weight categories, genders or sites. Concentrations of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) were significantly greater in the elderly than the adults (p 0.001). Ghrelin and fasting leptin concentrations differed significantly between weight categories, genders and sites (p 0.05), while GLP-1 and PYY concentrations differed significantly between genders only (p 0.05). Compared to NP drinks, HP drinks significantly increased postprandial GLP-1 and PYY (p 0.001). Advanced age was concomitant with reduced appetite and elevated anorectic hormone release, which may contribute to the development of malnutrition. In addition, appetite hormone concentrations differed between weight categories, genders and geographical locations
Co-culture of primary rat hepatocytes with rat liver epithelial cells enhances interleukin-6-induced acute-phase protein response
Three different primary rat hepatocyte culture methods were compared for their ability to allow the secretion of fibrinogen and albumin under basal and IL-6-stimulated conditions. These culture methods comprised the co-culture of hepatocytes with rat liver epithelial cells (CC-RLEC), a collagen type I sandwich culture (SW) and a conventional primary hepatocyte monolayer culture (ML). Basal albumin secretion was most stable over time in SW. Fibrinogen secretion was induced by IL-6 in all cell culture models. Compared with ML, CC-RLEC showed an almost three-fold higher fibrinogen secretion under both control and IL-6-stimulated conditions. Induction of fibrinogen release by IL-6 was lowest in SW. Albumin secretion was decreased after IL-6 stimulation in both ML and CC-RLEC. Thus, cells growing under the various primary hepatocyte cell culture techniques react differently to IL-6 stimulation with regard to acute-phase protein secretion. CC-RLEC is the preferred method for studying cytokine-mediated induction of acute-phase proteins, because of the pronounced stimulation of fibrinogen secretion upon IL-6 exposure under these conditions
Let thy food be thy medicineâŚ.when possible
There is no evidence that Hippocrates, although being credited for it, ever literally stated âlet thy food be thy medicine and thy medicine be thy foodâ. However, yet in line with Hippocratesâ philosophy, we are currently witnessing a reappraisal of the complementarity of nutrition and pharmacology. Recent studies not only underline the therapeutic potential of lifestyle interventions, but are also generating valuable insights in the complex and dynamic transition from health to disease. Next to this, nutritional biology can significantly contribute to the discovery of new molecular targets. It is clear that most of the current top-selling drugs used in chronic cardio-metabolic diseases modulate relatively late-stage complications, which generally indicate already longer existing homeostatic imbalances. Pharmacologists are increasingly aware that typical multifactorial disorders require subtle, multiple target pharmacological approaches, instead of the still often dominating âone disease - one target - one drugâ paradigm. This review discusses the recent developments in the pharma-nutrition interface and shows some relevant mechanisms, including receptors and other targets, and examples from clinical practice. The latter includes inflammatory diseases and progressive loss of muscle function. The examples also illustrate the potential of targeted combinations of medicines with nutrition and (or) other life-style interventions, to increase treatment efficacy and (or) reduce adverse effects. More attention to a potentially negative outcome of drug-food combinations is also required, as shown by the example of food-drug interactions. Together, the developments at the food-pharma interface underline the demand for intensified collaboration between the disciplines, in the clinic and in science.</p
The role of hypothalamic inflammation, the hypothalamicâpituitaryâadrenal axis and serotonin in the cancer anorexiaâcachexia syndrome
PURPOSE OF REVIEW: In cancer patients, the development of cachexia (muscle wasting) is frequently aggravated by anorexia (loss of appetite). Their concurrence is often referred to as anorexiaâcachexia syndrome. This review focusses on the recent evidence underlining hypothalamic inflammation as key driver of these processes. Special attention is given to the involvement of hypothalamic serotonin. RECENT FINDINGS: The anorexiaâcachexia syndrome is directly associated with higher mortality in cancer patients. Recent reports confirm its severe impact on the quality of life of patients and their families.Hypothalamic inflammation has been shown to contribute to muscle and adipose tissue loss in cancer via central hypothalamic interleukine (IL)1β-induced activation of the hypothalamicâpituitaryâadrenal axis. The resulting release of glucocorticoids directly stimulates catabolic processes in these tissues via activation of the ubiquitinâproteosome pathway. Next to this, hypothalamic inflammation has been shown to reduce food intake in cancer by triggering changes in orexigenic and anorexigenic responses via upregulation of serotonin availability and stimulation of its signalling pathways in hypothalamic tissues. This combination of reduced food intake and stimulation of tissue catabolism represents a dual mechanism by which hypothalamic inflammation contributes to the development and maintenance of anorexia and cachexia in cancer. SUMMARY: Hypothalamic inflammation is a driving force in the development of the anorexia-cachexia syndrome via hypothalamicâpituitaryâadrenal axis and serotonin pathway activation
The Use of Proton Pump Inhibitors May Increase Symptoms of Muscle Function Loss in Patients with Chronic Illnesses
Long-term use of proton pump inhibitors (PPIs) is common in patients with muscle
wasting-related chronic diseases. We explored the hypothesis that the use of PPIs may contribute to
a reduction in muscle mass and function in these patients. Literature indicates that a PPI-induced
reduction in acidity of the gastrointestinal tract can decrease the absorption of, amongst others,
magnesium. Low levels of magnesium are associated with impaired muscle function. This
unwanted side-effect of PPIs on muscle function has been described in different disease backgrounds.
Furthermore, magnesium is necessary for activation of vitamin D. Low vitamin D and magnesium
levels together can lead to increased inflammation involved in muscle wasting. In addition, PPI use
has been described to alter the microbiotaâs composition in the gut, which might lead to increased
inflammation. However, PPIs are often provided together with nonsteroidal anti-inflammatory drugs
(NSAIDs), which are anti-inflammatory. In the presence of obesity, additional mechanisms could
further contribute to muscle alterations. In conclusion, use of PPIs has been reported to contribute to
muscle function loss. Whether this will add to the risk factor for development of muscle function loss
in patients with chronic disease needs further investigation
The role of hypothalamic inflammation, the hypothalamicâpituitaryâadrenal axis and serotonin in the cancer anorexiaâcachexia syndrome
PURPOSE OF REVIEW: In cancer patients, the development of cachexia (muscle wasting) is frequently aggravated by anorexia (loss of appetite). Their concurrence is often referred to as anorexiaâcachexia syndrome. This review focusses on the recent evidence underlining hypothalamic inflammation as key driver of these processes. Special attention is given to the involvement of hypothalamic serotonin. RECENT FINDINGS: The anorexiaâcachexia syndrome is directly associated with higher mortality in cancer patients. Recent reports confirm its severe impact on the quality of life of patients and their families.Hypothalamic inflammation has been shown to contribute to muscle and adipose tissue loss in cancer via central hypothalamic interleukine (IL)1β-induced activation of the hypothalamicâpituitaryâadrenal axis. The resulting release of glucocorticoids directly stimulates catabolic processes in these tissues via activation of the ubiquitinâproteosome pathway. Next to this, hypothalamic inflammation has been shown to reduce food intake in cancer by triggering changes in orexigenic and anorexigenic responses via upregulation of serotonin availability and stimulation of its signalling pathways in hypothalamic tissues. This combination of reduced food intake and stimulation of tissue catabolism represents a dual mechanism by which hypothalamic inflammation contributes to the development and maintenance of anorexia and cachexia in cancer. SUMMARY: Hypothalamic inflammation is a driving force in the development of the anorexia-cachexia syndrome via hypothalamicâpituitaryâadrenal axis and serotonin pathway activation
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