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The role of long‐term parenteral support in patients with underlying benign conditions who do not have intestinal failure (IF) is contentious, not least since there are clear benefits in utilising the oral or enteral route for nutritional support. Furthermore, the risks of long‐term home parenteral nutrition (HPN) are significant, with significant impacts on morbidity and mortality. There has, however, been a recent upsurge of the use of HPN in patients with conditions such as gastro‐intestinal neuromuscular disorders, opioid bowel dysfunction, disorders of gut–brain interaction and possibly eating disorders, who do not have IF. As a result, the European Society of Clinical Nutrition and Metabolism (ESPEN), the European Society of Neuro‐gastroenterology and Motility (ESNM) and the Rome Foundation for Disorders of Gut Brain Interaction felt that a position statement is required to clarify – and hopefully reduce the potential for harm associated with – the use of long‐term parenteral support in patients without IF. Consensus opinion is that HPN should not be prescribed for patients without IF, where the oral and/or enteral route can be utilised. On the rare occasions that PN commencement is required to treat life‐threatening malnutrition in conditions such as those listed above, it should only be prescribed for a time‐limited period to achieve nutritional safety, while the wider multi‐disciplinary team focus on more appropriate biopsychosocial holistic and rehabilitative approaches to manage the patient's primary underlying condition. [ABSTRACT FROM AUTHOR]

Summary: Rationale: This initiative is focused on building a global consensus around core diagnostic criteria for malnutrition in adults in clinical settings. Methods: In January 2016, the Global Leadership Initiative on Malnutrition (GLIM) was convened by several of the major global clinical nutrition societies. GLIM appointed a core leadership committee and a supporting working group with representatives bringing additional global diversity and expertise. Empirical consensus was reached through a series of face‐to‐face meetings, telephone conferences, and e‐mail communications. Results: A two‐step approach for the malnutrition diagnosis was selected, i.e., first screening to identify "at risk" status by the use of any validated screening tool, and second, assessment for diagnosis and grading the severity of malnutrition. The malnutrition criteria for consideration were retrieved from existing approaches for screening and assessment. Potential criteria were subjected to a ballot among the GLIM core and supporting working group members. The top five ranked criteria included three phenotypic criteria (weight loss, low body mass index, and reduced muscle mass) and two etiologic criteria (reduced food intake or assimilation, and inflammation or disease burden). To diagnose malnutrition at least one phenotypic criterion and one etiologic criterion should be present. Phenotypic metrics for grading severity as Stage 1 (moderate) and Stage 2 (severe) malnutrition are proposed. It is recommended that the etiologic criteria be used to guide intervention and anticipated outcomes. The recommended approach supports classification of malnutrition into four etiology‐related diagnosis categories. Conclusion: A consensus scheme for diagnosing malnutrition in adults in clinical settings on a global scale is proposed. Next steps are to secure further collaboration and endorsements from leading nutrition professional societies, to identify overlaps with syndromes like cachexia and sarcopenia, and to promote dissemination, validation studies, and feedback. The diagnostic construct should be re‐considered every 3–5 years. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Insulin effects reportedly involve reactive oxygen species (ROS) and oxidative stress in vitro, but skeletal muscle oxidative stress is an emerging negative regulator of insulin action following high-fat feeding. NEFA may enhance oxidative stress and insulin resistance. We investigated the acute impact of insulin with or without NEFA elevation on muscle ROS generation and insulin signalling, and the potential association with altered muscle mitochondrial function. Methods: We used hyperinsulinaemic-euglycaemic clamping, 150 min, without or with lipid infusion to modulate plasma NEFA concentration in lean rats. Results: Insulin and glucose (Ins) infusion selectively enhanced xanthine oxidase-dependent muscle ROS generation. Ins with lipid infusion (Ins+NEFA) lowered whole-body glucose disposal and muscle insulin signalling, and these effects were associated with high muscle mitochondrial ROS generation and activation of the proinflammatory nuclear factor-κB inhibitor (IκB)-nuclear factor-κB (NFκB) pathway. Antioxidant infusion prevented NEFA-induced systemic insulin resistance and changes in muscle mitochondrial ROS generation, IκB-NFκB pathway and insulin signalling. Changes in insulin sensitivity and signalling were independent of changes in mitochondrial enzyme activity and ATP production, which, in turn, were not impaired by changes in ROS generation under any condition. Conclusions/interpretation: Acute muscle insulin effects include enhanced ROS generation through xanthine oxidase. Additional NEFA elevation enhances mitochondrial ROS generation, activates IκB-NFκB and reduces insulin signalling. These alterations are not associated with acute reductions in mitochondrial enzyme activity and ATP production, and are reversed by antioxidant infusion. Thus, NEFA acutely cause systemic and muscle insulin resistance by enhancing muscle oxidative stress through mitochondrial ROS generation and IκB-NFκB activation. [ABSTRACT FROM AUTHOR]

Inflammation and oxidative stress are important contributors to atherosclerosis initiation, progression, and clinical complications. The inflammatory process, which is promoted by several cardiovascular risk factors, involves both a local microinflammatory response and a systemic low-grade inflammation. Oxidative stress significantly contributes to vascular damage, amplifies the inflammatory response, and is responsible for low-density lipoprotein (LDL) oxidation, which triggers plaque formation. Several nutritional strategies that can impact inflammation and oxidative stress have been identified. Omega-3 fatty acids, antioxidant vitamins, carotenoids, and polyphenols may all influence atherosclerosis initiation and clinical progression. Large-scale clinical trials have been conducted to assess the effects of some of these nutritional principles on selected cardiovascular endpoints. Optimization of nitric oxide bioavailabilily to the vessel wall by nutritional modulation of its production may represent a winning strategy in primary and secondary prevention of cardiovascular disease. Based on clinical evidence, routine antioxidant supplementation is currently not recommended in the general population for the primary and secondary prevention of cardiovascular disease. Instead the benefits of a diet rich in fruit and vegetables should be emphasized in nutritional counseling. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Hyperfibrinogenaemia and albuminuria are cardiovascular risk factors, often coexisting in diabetic and non-diabetic people. Albuminuria in turn is associated with a compensatory albumin overproduction in non-diabetic patients. It is not known whether the presence of albuminuria in patients with type 2 diabetes mellitus is associated with greater albumin and fibrinogen production rates than in normoalbuminuric patients. Subjects, materials, and methods: Using leucine isotope methods, we measured fractional and absolute synthesis rates (FSR, ASR) of albumin and fibrinogen in post-absorptive type 2 diabetic patients with either normal (n=11) or increased (n=10) urinary albumin excretion. Results: In albuminuric patients, albumin FSR (16.2±1.5%/day) and ASR (20.5±1.9 g/day) were greater (p<0.02 and p<0.05, respectively) than in normoalbuminuric patients (FSR=11.5±1.1%/day; ASR=15.7±1.2 g/day). Fibrinogen FSR was similar between patients with normal and increased albumin excretion, but concentration, the circulating pool and ASR of fibrinogen were 40 to 50% greater (p<0.035) in patients with albuminuria. Albuminuria was positively correlated with albumin ASR, with fibrinogen concentration, the fibrinogen pool and ASR, whereas albumin synthesis was inversely correlated with calculated oncotic pressure. Conclusions/interpretation: Synthesis of albumin and fibrinogen is upregulated in type 2 diabetic patients with increased urinary albumin excretion. Albuminuria is associated with enhanced fibrinogen and albumin synthesis. [ABSTRACT FROM AUTHOR]

Presents information on a study that examined the effect of caloric restriction on gene transcript profiles and mitochondrial function in skeletal muscle of rats. Methodology of the study; Results and discussion on the study.

Presents a study that determined the impact of a high-fat diet on rat skeletal muscle gene expression and mitochondrial function. Effect of high-fat diet (HFD) on the health of human and animal species; Comparison of gene transcript patterns between control and HFD groups; Changes in several gene transcripts induced by high-fat diet and antioxidant intervention.

Although protein wasting and reduced amino acid concentrations are common findings in glucagonoma patients, the mechanisms underlying these alterations are unclear. Therefore, we studied basal postabsorptive leucine, phenylalanine and tyrosine turnover following L-[D3]-Leucine, L-[D5]-Phenylalanine and L-[D2]-Tyrosine i. v. infusions in one male and one female patient with glucagonoma, compared with healthy control volunteers. Plasma amino acid concentrations were reduced (–40 to 80 %, δ > 2 SD vs control subjects) in both patients. Plasma leucine, phenylalanine and tyrosine rates of appearance in patients with glucagonoma were similar to values in the control subjects, except leucine rate of appearence in the female patient with glucagonoma ( + &30 %, d > 2 SD). In contrast, the intracellular leucine rate of appearence, reflecting protein degradation, was considerably increased in both patients ( + 60–80 %, δ > 2 SD). Phenylalanine hydroxylation was moderately higher only in the male patient with glucagonoma ( + &30 %, d > 2 SD). Leucine, phenylalanine and tyrosine clearances ( + 100–300 %), as well as phenylalanine hydroxylative clearance ( + 75–100 %) were also increased in the patients. In conclusion, whole-body protein breakdown is enhanced in patients with glucagonoma compared with healthy control subjects. Phenylalanine hydroxylative clearance is also higher. Reduced plasma amino acid concentrations are probably due, at least in part, to their increased clearance. These alterations could contribute to the determination of the catabolic state of the glucagonoma syndrome. [Diabetologia (1999) 42: 326–329] [ABSTRACT FROM AUTHOR]

Presents information on a study which assessed the reliability of arterial ketoisocaproate as a predictor of leucine enrichment in the hepatic and femoral veins. Methods; Results and discussion; Conclusion.

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