Effects of an individualised nutritional intervention to tackle malnutrition in nursing homes: a pre-post study.

PURPOSE: Individualised interventions are recommended to tackle malnutrition in older adults, but approaches for nursing home (NH) residents are scarce. This study investigated the effects of an individualised nutritional intervention in NH residents with (risk of) malnutrition. METHODS: In a pre-post study, 6 weeks (w) of usual care were followed by 6w of intervention. The intervention consisted of up to three supplement modules (sweet and savoury protein creams and protein-energy drink, single or combined) and, if required, reshaped texture-modified meals (RTMM). RESULTS: Fifty residents completed the study (84 ± 8 years, 74% female). One-third (32%) received RTMM. Additional 258 ± 167 kcal/day and 23 ± 15 g protein/day were offered. Mean daily energy intake increased by 207 (95%CI 47-368, p = 0.005) kcal and protein intake by 14 (7-21, p < 0.001) g (w12 vs w1). Quality of life (QoL) increased in the subscale "care relationship" (+ 9 (3-15) points, p = 0.002, w12 vs w6). Body weight, handgrip strength, and other QoL subscales did not change. CONCLUSION: Our intervention improved dietary intake and one QoL subscale in NH residents with (risk of) malnutrition. As a next step, randomized controlled trials are needed to investigate the impact of individualised interventions more comprehensively.

Inositol phospho-oligosaccharides from rat fibroblasts and adipocytes stimulate 3-O-methylglucose transport.

Inositol phospho-oligosaccharides (IPOs), which are released from liver membranes upon stimulation by insulin, mimic a wide spectrum of insulin effects in different cells, but not the stimulation of glucose transport. We investigated whether other insulin-sensitive tissues release glucose transport-stimulating IPOs and whether this is related to the human insulin receptor isoform-A or -B (HIR-A or HIR-B). Rat1 fibroblasts overexpressing HIR-A or -B (rat1-HIR cells) were labelled with [3H]glucosamine, [3H]mannose or myo-[3H]inositol. IPOs from the cell supernatant were partially purified by an AG1X2 anion-exchange column, and fractions were eluted at different pH values (pH 3, pH 2 and pH 1.3). The label from glucosamine, mannose and myo-inositol appeared predominantly in the pH 2 fraction. The biological activity of the fractions was determined by measuring 3-O-methylglucose transport and lipogenesis in fat cells. Using the pH 2 fraction from the supernatant of rat1-HIR fibroblasts, insulin increased the release of 3-O-methylglucose-transport-stimulating activity (HIR-A: without insulin, 22.4 +/- 5.4%; with insulin 54.0 +/- 8.4%; HIR-B: without insulin 21.6 +/- 7.5%, with insulin, 44.7 +/- 10.6%, given as a percentage of equilibrium glucose transport reached after 4 s) and lipogenesis-stimulating activity (HIR-A: without insulin, 1.24 +/- 0.17; with insulin, 4.69 +/- 0.2; HIR-B: without insulin, 1.34 +/- 0.18; with insulin, 4.98 +/- 0.31, given as nmol of [3H]glucose converted into lipids/min per 10(6) cells). Analogous experiments were performed with isolated rat fat cells expressing the physiological level of insulin receptors. Upon insulin stimulation of fat cells in the presence of 2.5 mM mannose, the release of 3-O-methylglucose-transport-stimulating activity was detected (for purified supernatant of adipocytes without insulin, 6.9 +/- 1.12%; with insulin, 41.0 +/- 3.6%) and lipogenesis-stimulating activity (without insulin, 0.93 +/- 0.17, with insulin 2.96 +/- 0.31 nmol/min per mg). These data suggest (1) that adipocytes and rat1-HIR fibroblasts release IPOs that are able to stimulate glucose transport, (2) that both insulin receptor isoforms (HIR-A and HIR-B) mediate the effect of insulin on IPO release, and (3) that overexpression of insulin receptors increases the basal release of IPOs.

New site-directed reversible inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase.

1. CoA-thioether analogues of 3-hydroxy-3-methylglutaryl-CoA containing an additional methyl group at positions 2, 6(methyl at C3) or 4 of the acyl residue were prepared. To probe for hydrophobic interaction, their inhibitory properties were determined with 3-hydroxy-3-methylglutaryl-CoA reductase purified from baker's yeast. The CoA-thioethers were purely competitive inhibitors whose affinity to the reductase was near to that of the physiological substrate. 2. CoA-sulfoxides derived from the CoA-thioethers displayed affinities to the reductase superior to that of the physiological substrate (Km = 7 microM). Depending on the degree of recognition of diastereomers by the enzyme, the inhibitor constants of the two best inhibitors vary from Ki = 200 nM and Ki = 80 nM (diastereomeric mixtures) to 25 nM and 20 nM, respectively (if only one diastereomer would interact with the enzyme).

Enhanced proliferation of coronary endothelial cells in response to growth factors is synergized by hemodialysate compounds in vitro.

Using capillary endothelial cells from the coronary system of guinea pig heart, we have devised an in vitro assay suitable for measuring proliferative and growth-promoting effects mediated by drugs and growth factors. In this assay, hemodialysate and fractions isolated from it--consisting exclusively of low-molecular-weight compounds from calf blood--stimulate the proliferation of coronary endothelial cells. This effect is not a trivial nutritive one. Furthermore, in respect to the stimulation of proliferation, hemodialysate synergizes with epidermal growth factor, basic fibroblast growth factor, and endothelial cell growth factor, but not with insulin, which shows no proliferative effect in our system. From data obtained by analysis of hemodialysate fractions, it is deduced that the active compounds are strongly negatively charged oligosaccharides with a molecular weight of apparently 3000 Dalton. The synergistic effect of hemodialysate compounds on proliferation of endothelial cells as well as their previously demonstrated insulin-like activity is believed to explain the therapeutic efficacy of hemodialysate in cases of impaired wound healing and occlusive diseases.