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Objective: Cachexia, or disease-related loss of muscle mass, is a complication of chronic liver disease that modifies its clinical course. The aim of this study was to determine whether improvement in liver function and cachexia through control of the hepatitis B virus (HBV) increases skeletal muscle mass., Methods: The blood tests and cross-sectional area (mm(2)) of the psoas major muscle on computed tomography were measured before and after long-term entecavir therapy (median, 39 mo; range, 14-76 mo) in patients with hepatitis B (17 men, 13 women; mean age, 63 ± 13 y)., Results: The anti-HBV effect was good in 30 patients given entecavir, and most patients had undetectable serum HBV-DNA levels (93%) and alanine aminotransferase normalization (83%) within a median of 32 mo. Overall, no significant change in the area of the psoas major muscle was seen in any of the patients, although a significant increase was seen when limited to cases of protein malnutrition defined as serum albumin (Alb) <4 g/dL. A positive correlation was seen for the amount of change (Δ) in the psoas major muscle and the amount of change (Δ) in Alb., Conclusions: The present findings suggest that skeletal muscle mass may fluctuate in parallel with Alb levels. An improvement in low muscle mass may thus be expected from antiviral therapy for viral liver disease, especially in patients with cachexia., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Objective: To explain why vegetarian subjects develop morbidity and mortality from cardiovascular diseases unrelated to vitamin B status and Framingham criteria., Methods: A study of 24 rural male subjects 18 to 30 y old and 15 urban male controls was conducted in the Sahel region of Chad. Food consumption was determined from a dietary questionnaire, and overall health status was assessed by body weight, body mass index, serum albumin, plasma transthyretin, urinary nitrogen, and creatinine. Plasma lipids, vitamins B6, B9 and B12, homocysteine, and related sulfur amino acids were measured as selected cardiovascular disease risk factors., Results: Body weight, body mass index, blood, and urinary markers of protein status were significantly lower, with an estimated 10% decrease of lean body mass in the study group compared with urban controls. Neither lipid fractions nor plasma levels of vitamins B6, B9, and B12 were significantly different between the two groups. Although the mean consumption of sulfur amino acids (10.4 mg·kg(-1)·d(-1)) by rural subjects was significantly below the recommended dietary allowances (13 mg·kg(-1)·d(-1)), plasma methionine values were similar in the two groups. In contrast, homocysteine concentration was significantly increased (18.6 μmol/L, P < 0.001), and the levels of cysteine and glutathione were significantly decreased in the study group, demonstrating inhibition of the trans-sulfuration pathway. The strong negative correlation (r = -0.71) between transthyretin and homocysteine implicated lean body mass as a critical determinant of hyperhomocysteinemia., Conclusion: The low dietary intake of protein and sulfur amino acids by a plant-eating population leads to subclinical protein malnutrition, explaining the origin of hyperhomocysteinemia and the increased vulnerability of these vegetarian subjects to cardiovascular diseases., (Published by Elsevier Inc.)

Objective: The effect of Lactobacillus casei CRL 431 immunomodulatory activity on inflammation and coagulation during pneumococcal pneumonia was investigated in malnourished mice., Methods: Weaned mice were malnourished after they consumed a protein-free diet for 21 d. Malnourished mice were treated for 7 d with a balanced conventional diet (BCD) with L. casei supplementation (BCD+Lc) or without it. The malnourished control group received only a protein-free diet whereas well-nourished control (WNC) mice consumed BCD ad libitum. Mice were challenged by the intranasal route with pneumococci at the end of each dietary treatment. Lung injury, leukocyte recruitment, cytokine production, coagulation tests, and fibrin(ogen) deposition in lungs were evaluated., Results: Malnourished control mice showed impaired leukocyte recruitment and cytokine production, and more severe lung injuries when compared with WNC mice. Coagulation tests were significantly impaired in malnourished control group versus WNC group. Repletion with BCD or BCD+Lc improved these parameters, but only BCD+Lc mice achieved the values of WNC mice. In addition, the interleukin-10 level was higher in the BCD+Lc group than in the WNC group., Conclusion: Repletion with supplemental L. casei accelerated recovery of the defense mechanisms against pneumococci by inducing different cytokine profiles. These cytokines would be involved in the improvement of the immune response and in the induction of a more efficient regulation of the inflammatory process, limiting the injury caused by infection.

The head and neck cancer patient often presents with both protein malnutrition and trace element deficiencies. Zinc has been found to be deficient in many head and neck cancer patients. In this study, pretreatment zinc status and nutritional status (measured by the Prognostic Nutritional Index [PNI]) were correlated with clinical outcomes in 47 patients. The patients were followed-up for a median of 52 mo from the time of enrollment. Our results showed that the tumor size and overall stage correlated significantly to zinc status whereas no such correlation was seen with PNI, alcohol intake, or smoking in our subjects. The results also showed that impaired zinc status was associated with an increased number of treatment morbidities, unplanned hospitalizations, and treatment delays (P < 0.05). Nutritional status was not associated with any studied outcome variable. The disease-free interval was highest for the group which had both zinc-sufficient and nutrition-sufficient status. Although our data do not prove conclusively, they do suggest that impaired zinc status at presentation may contribute to treatment morbidity, and that for an optimal mean disease-free interval, a sufficient zinc and nutritional status is required.

The aim of this study was to determine if intraperitoneal administration of a nucleoside-nucleotide mixture would affect small intestinal morphology, bone marrow cell number, and DNA content in protein-deficient mice subjected to acute bacterial infection. Mice were randomized into two groups and orally fed protein-free diet or nucleotide-free 20% casein diet for 10 d. The mice in each group were divided into two subgroups and intraperitoneally administered 0.35 mL saline or nucleoside-nucleotide mixture (17.5 mL/kg body weight) for 10 d. On day 10, one subgroup from each major dietary group was either inoculated intravenously with methicillin-resistant Staphylococcus aureus or saline. Three days later, small intestinal morphology, bone marrow cell number, and DNA content were evaluated in infected and noninfected mice. Protein-deficiency in association with infection significantly (P < 0.05) reduced body weight, small intestinal weight, crypt depth, villous height, and wall thickness. All dietary groups exhibited similar small intestinal DNA and protein contents (protein:DNA ratio, RNA:DNA ratio) at 3 d postinfection. However, small intestinal RNA content in the infected protein-free dietary group administered nucleoside-nucleotide mixture was higher (P < 0.05) and tended to be higher relative to the infected nucleotide-free 20% casein group administered nucleoside-nucleotide mixture compared with the rest of the groups. In the infected protein-free dietary group administered nucleoside-nucleotide mixture, bone marrow cell number and bone marrow DNA content were higher (P < 0.05) relative to the infected protein-free dietary group, nucleotide-free 20% casein diet administered saline, or nucleoside-nucleotide mixture, respectively. We conclude that intraperitoneal administration of nucleoside-nucleotide mixture may stimulate bone marrow cell proliferation, DNA content, and small intestinal RNA content during periods of relative deficiency such as protein-deficiency in combination with infection.

Primary and secondary immune responses to low doses of sheep red blood cells (SRBC) were investigated in well-fed first-degree offspring of three groups of protein-deficient mice (PD) and in well-fed first-degree offspring of well-fed mice (ND). The offspring of malnourished males and malnourished females had the highest level of primary anti-SRBC antibodies, followed by the offspring of well-fed males and malnourished females, which also had a significantly higher primary anti-SRBC antibody titer than the ND mice. The antibody titer to SRBC of the offspring of malnourished males and well-fed females was, however, not significantly different from that of the ND mice. Following the administration of Plasmodium yoelii, the offspring of the malnourished males and females had the highest mean percentage of parasitemia, followed by the offspring of the well-fed males and malnourished females. The offspring of malnourished males and well-fed females had a mean percentage of parasitemia very close to that of the control group. The study confirms that impaired immunocompetence caused by intrauterine protein depletion may be so permanent as to affect the next generation as well, thereby giving an immunologic profile similar to that of the undernourished mothers.

The relation of serum very low density lipoproteins (VLDL) to hepatic steatosis was studied during protein malnutrition followed by refeeding of a balanced diet in growing rats. A control group was fed a balanced diet containing 15% casein for 42 days. Two depleted groups were fed low protein diets containing 2% casein (group C) or 5% gluten (group GI) (protein malnutrition phase) for 28 days and then were fed the balanced diet for 14 days (refeeding phase). The concentrations of phospholipids and proteins in both liver and serum VLDL were decreased during protein malnutrition, whereas triacylglycerols, unesterified cholesterol, and cholesteryl esters were higher in the liver and lower in the serum VLDL in the C and GI groups compared with the control group. There was a significant inverse relation between serum VLDL apolipoproteins and liver triacylglycerols on the one hand and between serum VLDL triacylglycerols and liver triacylglycerols on the other hand, in both depleted groups, although this relation was less important in the GI group. The major fatty acid levels of liver triacylglycerols were negatively correlated with those of serum VLDL during protein malnutrition. Our results show that in spite of a similar fatty acid intake, protein malnutrition involved an important decrease in essential fatty acids in VLDL triacylglycerols and phospholipids. Moreover, triacylglycerol accumulation was accompanied by increases in unesterfied cholesterol and cholesteryl esters in the liver of rats fed low protein diets, especially with 5% gluten. Hence, the hepatic steatosis was not entirely attributable to impaired transport of triacylglycerols by VLDL.