Unveiling the Evidence for the Use of Pulses in Managing Type 2 Diabetes Mellitus: A Scoping Review.

Management of type 2 diabetes mellitus (T2DM) is a pressing global healthcare challenge. Innovative strategies that integrate superior medical and nutritional practices are essential for holistic care. As such, pulse consumption is encouraged for its potential benefit in reducing hypercholesterolaemia, dyslipidaemia, and triglyceride levels, as well as enhancing glycaemic control. This scoping review aims to assess the depth of evidence supporting the recommendation for pulse consumption in T2DM management and to identify gaps in the existing literature. We conducted a comprehensive search across the databases MEDLINE, Global Health, EMBASE, CINAHL, Web of Science, and the Cochrane Library (up to July 2023). We included population-based studies of any design, and excluded review-style articles. Articles published in languages other than English were also excluded. From the 2449 studies initially identified, 28 met our inclusion criteria. Acute postprandial trials demonstrated improved glucose responses and enhanced insulin responses to pulse-based intervention. Meanwhile, long-term trials reported meaningful improvements in T2DM indicators such as haemoglobin A1C (HbA1c), fasting glucose, fasting insulin, C-peptide, and markers of insulin resistance like homeostatic model assessment (HOMA). Integrating more pulses into the diets of diabetic individuals might offer an efficient and cost-effective strategy in the global initiative to combat T2DM.

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression.

The mechanism by which high fat-diet induced obesity affects cardiac protein expression is unclear, and the extent to which this is modulated by prebiotic treatment is not known. These outcomes were assessed in rats initially fed a high-fat diet, then the top 40% weight gain group were randomly allocated to control (CON), high-fat (HF) and HF supplemented with fructooligosaccharide (32 g; HF-FOS) treatments for 12 weeks (n = 10/group). At sacrifice, left ventricles were either frozen or preserved in formalin. Serum was stored for glucose and insulin measurements. Protein spectra was obtained using an Orbitrap analyzer, processed with Sequest and fold changes assessed with Scaffold Q +. Treatment effects for body weights, glucose and insulin were assessed using one-way ANOVA, and the differential protein expression was assessed by a Mann-Whitney U test. The Database for Annotation, Visualization and Integrated Discovery and the Kyoto Encyclopedia of Genes and Genomes identified pathways containing overrepresented proteins. Hematoxylin and eosin sections were graded for hypertrophy and also quantified; differences were identified using Chi-square analyses and Mann-Whitney U tests. HF diet fed rats were significantly (p < 0.05) heavier than CON, and 23 proteins involved in mitochondrial function and lipid metabolism were differentially expressed between HF and CON. Between HF-FOS and HF, 117 proteins involved in contractility, lipid and carbohydrate metabolism were differentially expressed. HF cardiomyocytes were significantly (p < 0.05) more hypertrophic than CON. We conclude that high-fat feeding and FOS are associated with subcellular deviations in cardiac metabolism and contractility, which may influence myocardial function and alter the risk of cardiovascular disease.

Carbohydrate Replacement of Rice or Potato with Lentils Reduces the Postprandial Glycemic Response in Healthy Adults in an Acute, Randomized, Crossover Trial.

Background: The postprandial blood glucose response (PBGR) following carbohydrate replacement of high-glycemic index (GI) foods with pulses, in a mixed meal, has not been accurately defined. Objective: We aimed to determine the extent to which PBGR and relative glycemic response (RGR) are lowered when half of the available carbohydrate (AC) from rice or potato is replaced with cooked lentils. Methods: Using a crossover design, 2 groups of 24 healthy adults randomly consumed 50 g AC from control white rice alone [mean ± SD body mass index (BMI, in kg/m2): 24.3 ± 0.5; mean ± SD age: 27.7 ± 1.2 y], instant potato alone (BMI: 24.0 ± 0.5; age: 27.4 ± 1.2 y), or the same starch source in a 50:50 AC combination with each of 3 types of commercially available lentils (large green, small green, split red). Fasting and postprandial blood samples were analyzed for glucose and insulin, and used to derive incremental area under the curve (iAUC), RGR, and maximum concentration (Cmax). Treatment effects were assessed with the use of repeated-measures ANOVA within the rice and potato treatments. Results: In comparison to rice alone, blood glucose iAUC and Cmax (P < 0.001) were lowered after consumption of rice with large green (P = 0.057), small green (P = 0.002), and split red (P = 0.006) lentils. Blood glucose iAUC and Cmax were also significantly lowered (P < 0.0001) after consumption of potato combined with each lentil, compared to potato alone. Plasma insulin iAUC and Cmax were significantly (P < 0.001) decreased when lentils were combined with potato, but not with rice. The RGRs of rice and potato were lowered by ∼20% and 35%, respectively, when half of their AC was replaced with lentils. Conclusions: Replacing half of the AC from high-GI foods with lentils significantly attenuates PBGR in healthy adults; this can contribute to defining a health claim for pulses and blood glucose lowering. This trial was registered at clinicaltrials.gov as NCT02426606.

A maternal high-fat, high-sucrose diet alters insulin sensitivity and expression of insulin signalling and lipid metabolism genes and proteins in male rat offspring: effect of folic acid supplementation.

A maternal high-fat, high-sucrose (HFS) diet alters offspring glucose and lipid homoeostasis through unknown mechanisms and may be modulated by folic acid. We investigated the effect of a maternal HFS diet on glucose homoeostasis, expression of genes and proteins associated with insulin signalling and lipid metabolism and the effect of prenatal folic acid supplementation (HFS/F) in male rat offspring. Pregnant Sprague-Dawley rats were randomly fed control (CON), HFS or HFS/F diets. Offspring were weaned on CON; at postnatal day 70, fasting plasma insulin and glucose and liver and skeletal muscle gene and protein expression were measured. Treatment effects were assessed by one-way ANOVA. Maternal HFS diet induced higher fasting glucose in offspring v. HFS/F (P=0·027) and down-regulation (P<0·05) of genes coding for v-Akt murine thymoma viral oncogene homolog 2, resistin and v-Raf-1 murine leukaemia viral oncogene homolog 1 (Raf1) in offspring skeletal muscle and acetyl-CoA carboxylase (Acaca), fatty acid synthase and phosphatidylinositol-4,5-biphosphate 3-kinase, catalytic subunit ß in offspring liver. Skeletal muscle neuropeptide Y and hepatic Kruppel-like factor 10 were up-regulated in HFS v. CON offspring (P<0·05). Compared with CON, Acaca and Raf1 protein expression levels were significantly lower in HFS offspring. Maternal HFS induced higher homoeostasis model of assessment index of insulin resistance v. CON (P=0·030) and HFS/F was associated with higher insulin (P=0·016) and lower glucose (P=0·025). Maternal HFS diet alters offspring insulin sensitivity and de novo hepatic lipogenesis via altered gene and protein expression, which appears to be potentiated by folate supplementation.

Impact of ß2-1 fructan on faecal community change: results from a placebo-controlled, randomised, double-blinded, cross-over study in healthy adults.

Healthy adults (n 30) participated in a placebo-controlled, randomised, double-blinded, cross-over study consisting of two 28 d treatments (ß2-1 fructan or maltodextrin; 3×5 g/d) separated by a 14-d washout. Subjects provided 1 d faecal collections at days 0 and 28 of each treatment. The ability of faecal bacteria to metabolise ß2-1 fructan was common; eighty-seven species (thirty genera, and four phyla) were isolated using anaerobic medium containing ß2-1 fructan as the sole carbohydrate source. ß2-1 fructan altered the faecal community as determined through analysis of terminal restriction fragment length polymorphisms and 16S rRNA genes. Supplementation with ß2-1 fructan reduced faecal community richness, and two patterns of community change were observed. In most subjects, ß2-1 fructan reduced the content of phylotypes aligning within the Bacteroides, whereas increasing those aligning within bifidobacteria, Faecalibacterium and the family Lachnospiraceae. In the remaining subjects, supplementation increased the abundance of Bacteroidetes and to a lesser extent bifidobacteria, accompanied by decreases within the Faecalibacterium and family Lachnospiraceae. ß2-1 Fructan had no impact on the metagenome or glycoside hydrolase profiles in faeces from four subjects. Few relationships were found between the faecal bacterial community and various host parameters; Bacteroidetes content correlated with faecal propionate, subjects whose faecal community contained higher Bacteroidetes produced more caproic acid independent of treatment, and subjects having lower faecal Bacteroidetes exhibited increased concentrations of serum lipopolysaccharide and lipopolysaccharide binding protein independent of treatment. We found no evidence to support a defined health benefit for the use of ß2-1 fructans in healthy subjects.

ß2-1 Fructan supplementation alters host immune responses in a manner consistent with increased exposure to microbial components: results from a double-blinded, randomised, cross-over study in healthy adults.

ß2-1 Fructans are purported to improve health by stimulating growth of colonic bifidobacteria, increasing host resistance to pathogens and stimulating the immune system. However, in healthy adults, the benefits of supplementation remain undefined. Adults (thirteen men, seventeen women) participated in a double-blinded, placebo-controlled, randomised, cross-over study consisting of two 28-d treatments separated by a 14-d washout period. Subjects' regular diets were supplemented with ß2-1 fructan or placebo (maltodextrin) at 3×5 g/d. Fasting blood and 1-d faecal collections were obtained at the beginning and at the end of each phase. Blood was analysed for clinical, biochemical and immunological variables. Determinations of well-being and general health, gastrointestinal (GI) symptoms, regularity, faecal SCFA content, residual faecal ß2-1 fructans and faecal bifidobacteria content were undertaken. ß2-1 Fructan supplementation had no effect on blood lipid or cholesterol concentrations or on circulating lymphocyte and macrophage numbers, but significantly increased serum lipopolysaccharide, faecal SCFA, faecal bifidobacteria and indigestion. With respect to immune function, ß2-1 fructan supplementation increased serum IL-4, circulating percentages of CD282+/TLR2+ myeloid dendritic cells and ex vivo responsiveness to a toll-like receptor 2 agonist. ß2-1 Fructans also decreased serum IL-10, but did not affect C-reactive protein or serum/faecal Ig concentrations. No differences in host well-being were associated with either treatment, although the self-reported incidence of GI symptoms and headaches increased during the ß2-1 fructan phase. Although ß2-1 fructan supplementation increased faecal bifidobacteria, this change was not directly related to any of the determined host parameters.

Phenolic profiles of 20 Canadian lentil cultivars and their contribution to antioxidant activity and inhibitory effects on α-glucosidase and pancreatic lipase.

Phenolic extracts from 20 Canadian lentil cultivars (Lens culinaris) were evaluated for total phenolic contents and composition, antioxidant activities (DPPH, FRAP, ORAC), and inhibitory properties against α-glucosidase and pancreatic lipase. Twenty one phenolic compounds were identified in the present study, with the majority being flavonoids, including kaempeferol glycosides, catechin/epicatechin glucosides and procyanidins. These phenolic compounds not only contributed significantly to the antioxidant activities, but they were also good inhibitors of α-glucosidase and lipase, two enzymes, respectively, associated with glucose and lipid digestion in the human intestine, thus contributing significantly to the control of blood glucose levels and obesity. More interestingly, it was the flavonols, not the flavanols, which showed the inhibitory activities against α-glucosidase and pancreatic lipase. Our result provides supporting information for developing lentil cultivars and functional foods with improved health benefits and suggests a potential role of lentil consumption in managing weight and control of blood glucose.

Effect of domestic cooking on carotenoids, tocopherols, fatty acids, phenolics, and antioxidant activities of lentils (Lens culinaris).

The phytochemicals and antioxidant activity in lipophilic and hydrophilic (extractable and bound) fractions of lentils before and after domestic cooking were investigated. The hydrophilic fractions in lentils contributed much more to the antioxidant activity than the lipophilic fraction. The phenolic content of lentils was mainly composed of extractable compounds. Significant changes (P < 0.05) in carotenoid, tocopherol, total phenolic, and condensed tannin contents of both extractable and bound phenolics fractions, as well as in antioxidant activities, were found in lentils before and after cooking. More specifically, cooking was found to favor the release of carotenoids and tocopherols and flavonols (kaempferol glycosides), but led to losses of flavanols (monomeric and condensed tannin). Whereas reduced flavanols and other phenolic compounds may have negatively affected the antioxidant activity, other components, especially the lipophilic antioxidants, were increased. The present study suggests that incorporation of cooked lentils into the diet will not cause significant loss to the phytochemical antioxidants and thus will retain the potential health benefits.

The glycemic index of pigmented potatoes is related to their polyphenol content.

Polyphenol extracts from coloured fruits and vegetables inhibit α-glucosidase in vitro, however it is not known whether this translates into an attenuation of blood glucose response in vivo. We examined this relationship in a GI study by feeding coloured potatoes to 9 healthy volunteers. We also examined the in vitro inhibitory activity of potato anthocyanin extracts on rat intestinal α-glucosidase. Potatoes (Purple Majesty; Red-Y38; Yukon Gold and Snowden) were fed with skin after cooking in a convection oven, using a random block design and 50 g available carbohydrate. Glucose was used as the standard and venous blood collected at 0, 15, 30, 45, 60, 90, 120 min. Areas under the curve (AUC) for glucose and insulin were calculated, and GI and Insulin Index derived. Neither AUC for blood glucose response nor insulin was significantly different among the various potatoes studied. Although the mean GI (±SE) values for the potato types varied (purple = 77.0 ± 9.0; red = 78.0 ± 14.0; yellow = 81.0 ± 16.0; and white = 93.0 ± 17.0), these differences were not significantly different. The mean (±SE) polyphenol content (mg GAE/100 g DW) was 234 ± 28; 190 ± 15; 108 ± 39; 82 ± 1 for purple, red, yellow and white potatoes, respectively. There was a significant inverse correlation between polyphenol content and GI of the potatoes (r = -0.825; p < 0.05; n = 4). In vitro, polyphenol extracts of red and purple potatoes inhibited α-glucosidase by 37.4 ± 2.2% and 28.7 ± 3.2%, respectively. The GI of coloured potatoes is significantly related to their polyphenol content, possibly mediated through an inhibitory effect of anthocyanins on intestinal α-glucosidase.

Wound-healing activity of the skin of the common grape (Vitis Vinifera) variant, Cabernet Sauvignon.

The common Grape L. (Vitaceae) is regarded as an important medicinal plant. European healers have suggested the use of grapevine sap, juice, and whole grape in the treatment of pain, allergic reactions, inflammation, and to promote wound healing. We evaluated grape-skin powder for its wound-healing activity using an excision wound model in rats. Animals were randomly divided into three groups of six (n = 6) each. The test group animals were treated topically with the grape-skin powder (100 mg/kg/day). The controls and standard group animals were treated with petroleum jelly and mupirocin ointment respectively. Healing was assessed by the rate of wound contraction, period of epithelialization, and hydroxyproline content. On day 13, treatment of the wounds with grape-skin powder enhanced significantly the rate of wound contraction (100 %). Treated animals showed significant decrease in the epithelialization period (p < 0.000) and increase in the hydroxyproline content (p < 0.05) when compared to control and the standard. Histological analysis was also consistent with the proposal that grape-skin powder exhibits significant wound-healing potential. Increased rate of wound contraction, hydroxyproline content, and decrease in epithelialization time in the treated animals support the use of grape-skin powder in the management of wound healing.

Zinc supplementation, morbidity and growth in stunted Jamaican children

We investigated whether there was a morbidity or growth response to zinc supplementation of nutrition clinic attenders in Kingston, which would indicate zinc deficiency. Children selected were singletons aged 6 to 24 months and stunted (<2.0 sd length for age, NCHS references). They were stratified by gender and age (6-11, 12-17, 18-24 mo.) and randomly assigned to receive zinc supplementation (n=31) (5mg elemental zinc), or placebo (n=30) daily for 12 weeks. Adequately nourished comparison children (n=24) were recruited from a well-baby clinic. Caretakers were interviewed to obtain social background data. Anthropometric measurements were done on enrolment and after 6 weeks, 12 weeks and 12 months. A weekly questionnaire to determine the stunted children's health was given to the caretakers during the supplementation period. The zinc supplemented and placebo groups were very similar on enrolment. The adequately nourished children were significantly better socio-economic circumstances. Five placebo children, but no zinc supplemented children, were hospitalized during the supplemented period (Fisher's exact test, two-tailed, p=0.02), indicating reduced severity of illness with supplementation, which suggests a response to zinc deficiency. There were no significant differences in hair zinc content among the three groups. Regression analyses showed that there were no significant effects of supplementation of length, height or head circumference, or on the incidence of any symptom. Mean duration of the episodes were significantly shorter for skin rashes in the supplemented group compared with the placebo group (ANCOVA, P=0.02), and longer for vomiting (ANCOVA, p=0.02).(AU)

Zinc supplementation: effects on the growth and morbidity of undernourished Jamaican children

OBJECTIVE: We investigated whether there was a growth or morbidity response to zinc supplementation. DESIGN: The study was randomized, placebo-controlled, and double-blind. SETTING: Children were recruited at clinics in Kingston, Jamaica, and supplemented at home. SUBJECTS: Children selected were singletons aged 6-24 months, and stunted (< -2.0 s.d. length for age, NCHS references). They were stratified by sex and age and randomly assigned to receive zinc supplement (n = 31) or placebo (n = 30). Four children were excluded because of hospitalization; all others had all measurements. Adequately nourished children (n = 24) were recruited from a well-baby clinic. INTERVENTIONS: The supplement provided 5 mg elemental zinc in a syrup daily for 12 weeks; the placebo comprised the syrup only. MAIN OUTCOME MEASURES: Caretakers were interviewed to obtain social background data, number of clinic visits and hospitalizations. Anthropometric measurements were done on enrolment, and after 6 weeks, 12 weeks and 12 months. Children's health was determined by weekly questionnaire to caretakers of the undernourished groups during the supplementation period. RESULTS: The supplemented and placebo groups were similar on enrolment. The adequately nourished children were from significantly better socio-economic circumstances. Mean initial hair zinc content was 5.5 +/- 4.8 mumol/g (supplemented group) and 6.7 +/1 12.1 mumol/g (placebo) (n.s.). Regression analyses showed that there were no significant effects of supplementation on length, height or head circumference, nor on the incidence of any morbidity symptom. Mean duration of the episodes was significantly shorter for skin rashes in the supplemented group compared with the control group (ANCOVA, P = 0.02), and longer for vomiting (P = 0.02). The incidence of hospitalization was significantly greater in the control group (Fisher's exact test, P = 0.02). CONCLUSIONS: Zinc supplementation reduced the hospitalizations which probably reflect severity of morbidity, but did not improve growth.(Au)

Comparison of antioxidant status during recovery from malnutrition on a corn oil- or coconut oil-based diet - abstract

Children recovering from malnutrition are given a high-energy diet during the "catch-up" phase. Corn oil, a poly-unsaturated fatty acid (PUFA) rich vegetable oil, is used to supply 60 per cent of the energy in the recovery diets. Previous work suggests that this high intake of corn oil may be associated with a deterioration of antioxidant status. A normal antioxidant status is essential for protection against cell damage. We therefore compared indices of antioxidant status (whole blood gluthathione, GSH; plasma vitamen E; and urinary mercapturic acid outputs (UMCA) in two groups of malnourished children who had recovered on isocaloric diets containing either PUFA rich, corn oil (Control group) or coconut oil (test group), which is rich in saturated fatty acids. Both groups showed an initial normalisation of GSH and vitamin E levels; whereas the test group maintained normal levels, the control group showed a progressive decrease of both indices during recovery. At discharge the test group had GSH (2.7 ñ 0.08 vs 2.44 ñ 0.88 mmol/Lrbc, mean ñ SEM) and vitamen E (8.44 ñ 1.21 vs 7.38 ñ 1.01 mg/l), levels that were significantly higher (p< 0.05) that in the Control group. Several children in the Control group had vitamen E levels that were below the accepted normal range. At recovery, UMCA outputs of the Control group (4.85 ñ 0.55 umol/kg/24 hr) were further increased, and as such were significantly higher (p < 0.05) than the admission mean (3.32 ñ 0.54 umol/kg/24 hr). In the test group, mean discharge UMCA output (1.98 ñ 0.44 umol/kg/24 hr) was significantly lower than admission values, as well as the mean discharge UMCA output of the Control group. This suggests that the body's burden of compounds that require detoxification is significantly increased when malnourished children are rehabilitated on a diet rich in corn oil. Following recovery on the coconut oil diet, plasma cholesterol levels (2.30 ñ 0.15 mmol) were similar to the pre-treatment mean (2.15 ñ 0.11 mmol). However, plasma levels of triglycerides fell significantly (p < 0.05) with treatment (pre: 1.23ñ0.14; post 0.88ñ0.08 mmol). When given a diet that is not rich in PUFA, malnourished children are able to maintain their antioxidant status within the normal range. It is suggested that coconut oil be used routinely in the formulation of recovery diets for malnourished children (AU)

Vitamin E status in oedematous and non-oedematous malnourished children - abstract

The antioxidant function of vitamin E is essential for maintaining the integrity of cell membranes. During the early phase of recovery from severe malnutrition, we measured the plasma levels of Vitamin E in 58 children on admission (A), and after metabolic recovery (B). A total of 19 marasmic children, and 34 with oedematous malnutrition (19 with marasmic-kwashiorkor and 15 with kwashiorkor) were studied. A further group of 5 oedematous children who were clinically assessed as extremely sick received daily vitamin E supplements. The children were all fed on the same dietary regimen. The results indicated that although vitamin E intake was greater in the non-oedematous (marasmic) children, the rate of change of concentration in the plasma did not differ between the two groups. This could possibly be attributed to a difference in the absorption or utilization of the vitamin between the groups. In the group receiving supplements, there was a significant increase in plasma vitamin E concentration between A and B. However, the rate of increase and the concentration at B did not differ from that in the two groups of unsupplemented children. We conclude that in malnourished children: (1) plasma viatmin E levels are low on admission, (2) values normalize by time B, and (3) supplementation with alpha-tocopherol in oil did not affect the rate of increase in plasma vitamin E. The supplement did not seem to be bioavailable (AU)

Plasma iron, transferrin and transferrin saturation of severely malnourished Jamaican children - abstract

Mortality amongst severely malnourished children is often associated with an unusually high hepatic store of iron (Fe). Indeed, this excess Fe has been implicated in the aetiology of kwashiorkor. In order to examine the possibility that unbound Fe may be present in the plasma of malnourished Jamaican children, Fe and its transport protein, transferrin were measured. Transferrin saturation ( percentTS) was calculated from plasma Fe and transferrin levels. The measurements were also carried out in a control group of 23 healthy children who had presented for elective minor surgery. Plasma Fe levels (fg/dl) in children with marasmic-kwashiorkor (MK; n = 59. 69ñmeanñ), kwashiorkor (K, n = 37; 76ñ) and in those who died (D;n = 24: 111ñ) were not significantly different from the control group (C; 79ñ). In the marasmic group Fe levels (M;n = 63: 66ñ g/dl) were significantly lower than (p<0.05) than normal. In malnutrition, transferrin levels (mg/dl) were significantly lower (p<0.001) than normal: C - 232ñM - 170ñn = 66: MK - 110ñn = 61: K - 84ñn = 41: D - 77ñn = 24. In the marasmic group transferrin levels were significantly higher (p<0.001) than the other malnourished groups. percentTS was lowest in the marasmic group and highest in the group of children who died. At a percentTS of 30 percent, mortality was 5 per cent compared with a mortality of 24 per cent when percentTS was >90 per cent. It is concluded that oedematous malnourished Jamaican children have normal plasma levels of iron, but significantly reduced levels of circulating transferrin. The latter were more severely decreased in children with kwashiorkor and those who died. Elevated percentTS was associated with increased mortality. It is recommended that iron supplements be witheld during the early stages of resuscitation of the malnourished child (AU)

Antioxidant status of malnourished children

Free radicals, by virtue of their reactive nature, could account for the clinical features of kwashiorkor. These chemical species are produced in excess only after antioxidant defences fall. The possibility of this situation occuring in children with kwashiorkor was therefore investigated. Whole blood glutathione (GSH) levels were significantly decreased in children with kwashiorkor and marasmic-kwashiorkor. This indicates the presence of an overwhelming pro-oxidant stress. At a GSH level of 1.90 moles/Irbc (6.80 æmoles/gHb) oedema could be diagnosed with a sensitivity, specificity and positive accuracy of greater than 90 percent. GSH correlated inversely with the degree of oedema (r = -0.69). In children with maramus GSH was normal. Erythrocyte concentrations of NADPtot were normal in all children. The percentage of this nucleotide in the oxidised form ( percentNADP+/NADPtot) was normal in children with maramus, but abnormally elevated in oedematous children. This means that there is an acute change in the cellular redox in oedematous children, and implies that the cellular environment is oxidising. The activities of erythrocyte glutathione reductase, glutathione S-transferase (GST) and glyoxalase I were either normal or markedly elevated. Riboflavin status was poor. The end products of detoxification by GST, urinary mercapturic acids (UMCA), were between 3 and 5 times higher than normal. There were no intergroup differences. This suggests that the body's burden of toxins is significantly increased. During recovery from malnutrition, children with maramus showed a rapid restoration of normal antioxidant status, whereas those with oedematous malnutrition did so only after loss of oedema. This was followed by progressive, and unexpected, deterioration in antioxidant status: plasma vit. E and GSH levels decreased, and UMCA levels remained elevated. It was reasoned that the high PUFA content (60 percent )of the recovery diet may be a source of oxidative stress. In a second study the recovery diet contained an oil (coconut), rich in saturated fatty acids. On this diet children maintained normal levels of vit.E and GSH, and UMCA decreased significantly. This confirmed the high PUFA diet as a source of oxidative stress. Collectively, these data suggest that free radicals are involved in the aetiology and pathogenesis of kwashiorkor. It is recommended that: (1) whole blood levels of GSH be used in the diagnosis of oedematous malnutrition, and (2) coconut oil and antioxidants be used to treat malnourished children (AU)

Selenium status during recovery from malnutrition: effects of selenium supplementation - abstract

It was previously shown that malnourished Jamaican children often had evidence of selenium deficiency, viz. low erythrocyte glutathione peroxidase (RBC GSH Px) activity that correlated inversely with cardiothoracic ratio, and was particularly low in children who died. In this study, RBC GSH Px activity, plasma GSH Px activity and plasma selenium concentration were measured in 41 malnourished children on admission to hospital, and after recovery in weight-for-height. Plasma GSH Px activity and selenium concentrations were also measured longitudinally throughout recovery in a group of 24 initially selenium-deficient children, 17 of whom were given oral selenium supplements for the first 3 weeks. RBC GSH Px activity was low in all malnourished children, whether oedematous or not (Table). It did not change with recovery. Plasma GSH Px activity and plasma selenium concentration were low only in oedematous malnourished children. PEM GROUPS: control, marasmus, oedematous; ERYTHROCYTE GSH Px (U/gHb)- *36ñ2, 24ñ4, 21ñ3 respectively; PLASMA GSH Px act. (U/L) - 140ñ9, 142ñ15, 98ñ8 respectively, PLASMA SE CONCN. (æg/e) - 86ñ4, 76ñ12, 53ñ5. *meanñSEM. Selenium was associated with a rapid rise in both plasma GSH Px activity and plasma selenium concentration. The increase in plasma selenium was more dramatic (44 up to 144 æg/e in 6 days): the variability in plasma GSH Px activity was much greater, and they remained within the control range. The changes were sustained after supplementation ceased. We conclude that (1) selenium deficiency in malnourished Jamaican children is not reversed during 'recovery' on the conventional 'high energy' diet, (2) plasma selenium concentration responds rapidly to changes in selenium intake, and is a useful measure of selenium status, and (3) oral selenium supplements improve selenium status in children recovering from malnutrition (AU)

Erythrocyte clutathione reductase activity and riboflavin status in severely malnourished children - abstract

Erythrocyte glutathione reductase (EGR), cofactor is riboflavin (vit B2), functions together with glucose 6-phosphate dehydrogenase to maintain cellular levels of glutathione and thus the integrity of the erythrocyte. The compromised antioxidant status of severely malnourished children along with increased exposure to metabolic stress led us to postulate that EGR activity might be increased in malnutrition as a compensatory response to oxidative stress. We therefore measured EGR activity in 49 severly malnourished children on admission and again in 35 of these children at discharge. Erythocyte glutathione-reductase-activation-coefficient (ERGAC), an index of riboflavin status, was also assessed. Twenty-two healthy children served as controls (C). The malnourished group had significantly higher EGR activity (8.34 ñ 0.31 U/g Hb; mean ñ SEM) than the control group (6.63 ñ 0.23 U/g Hb). On admission, children with marasmus (M) had significantly higher EGR activities (8.95 ñ .046 U/g Hb) than children with marasmic kwashiorkor (MK: 8.08 ñ 0.67 U/g Hb) or kwashiorkor (K: 7.66 ñ 0.53 U/g Hb). At discharge, high levels of EGR were maintained in all groups. However, the kwashiorkor group showed a significant increase up to (10.37 + 0.41 U/g Hb). An EGRAC > 1.30 indicates riboflavin deficiency. Forty per cent of the controls as well as 50 percent of the malnourished children were deficient in riboflavin supplementation of the malnourished groups, the EGRAC fell to normal levels. We concluded (1) that EGR activity is increased in severly malnourished children; this may be as a result of increased metabolic stress, and (2) the riboflavine status of malnourished children improved significantly during their recovery (AU)

Superoxide dismutase activity in red cell fractions from malnourished children

Red cell superoxide dismutase activity (CuSODA) is thought to be influenced by dietary intakes of copper. To test this hypothesis CuSODA was measured in the newly formed cells of fifteen severely malnourished children, given either a basal diet or the basal diet and copper supplements, during recovery from PEM. Cells were density fractionated using a discontinous density gradient of Percoll. Published methods were inadequate hence a new method was developed. A density gradient of Percoll containing thirteen different layers, with a density range of 1.076 g/ml to 1.108 g/ml, was used to fractionate red cells from the severely malnourished children. CuSODA and hemaglobin levels were measured in each fraction of cells. No differences were found in the CuSODA of children given a copper supplement, in addition to their regualr feeds, and children not given copper supplement. There was a rapid proliferation of new cells approximately two weeks after admission, in both groups. At discharge this reverted to a normal distribution skewed to the right, similar to the pattern at admission. It is concluded that (1) severely malnourished Jamaican children are not generally copper deficient, (2) diets given during rehabilitation are sufficient to prevent clinical copper deficiency, and (3) the response to dietary intakes of copper by red cell superoxide dismutase is variable and may involve a reconstitution of an apo-enzyme (AU)

Superoxide dismutase in red cell fractions in severe malnutrition - abstract

When fed a milk-based diet, the red cell superoxide dismutase activity (CuSODA) of malnourished children decreased. Copper supplementation prevented the decrease. This led to the suggestion that red cell CuSODA represented recent copper intake. By separating red blood cells (RBC) into fractions of different ages and measuring the CuSODA of each, it should be possible to obtain an estimate of the copper status over the life span of the RBC. There is a strong correlation between the age of RBCs and their destiny: young cells being less dense than old cells. Percoll was used to develop a method to separate cells iospycnically. Thirteen fractions were prepared with densities between 1.076 g/ml. RBCs from malnourished and healthy children were fractionated by this method, and each fraction assayed for haemoglobin and CuSODA. The total CuSODA of whole blood from each subject was also measured. Mean (and standard error) whole blood CuSODA of 15 malnourished children on admission was 3,284ñ132 i.u./gm Hb. This correlated well (r=0.69) with the sum of CuSODA in the fractions of cells (3,187ñ112). In malnourished children, there was a preponderance of heavy (old) cells. However, there was no difference in the CuSODA between the different fractions. There was a slight decrease in the CuSODA with increasing density in blood taken from three healthy children. The control children had higher CuSODA in their lighter cells. This study has shown that severely malnourished children have a preponderance of heavy (old) cells. The fact that young, less dense cells had the same CuSODA as old (more dense) cells suggests that there is no change in the copper status of severely malnourished children in the four-month (120 days) period prior to their admission to hospital (AU)