Effects of plant and animal high protein diets on immune-inflammatory biomarkers: A 6-week intervention trial.

BACKGROUND & AIMS: Pro-inflammatory biomarkers are well-established contributors to insulin resistance and represent valid targets for diabetes management and prevention. Yet, little is known whether nutrition could play a role in modulating various aspects of immune-inflammatory responses. Our aim is to assess the effect of isocaloric animal and plant protein dietary interventions on selected biomarkers representing various immune-inflammatory pathways. METHODS: We enrolled 37 participants with type 2 diabetes (age 64 ± 6 years, body mass index 30.2 ± 3.6 kg/m2, glycated hemoglobin 7.0 ± 0.6%) who underwent an either high-animal protein (AP) or high-plant protein (PP) diet (30 E% protein, 40 E% carbohydrates, 30 E% fat) for 6-weeks. Clinical examinations were performed at beginning and end of the study. Levels of pro-inflammatory adipokines [chemerin, progranulin], cytokines [tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), soluble urokinase-type plasminogen activator receptor (suPAR), transforming growth factor beta 1 (TGF-ß1)], and proteins [calprotectin, lactoferrin and growth differentiation factor 15 (GDF-15)] were determined in blood serum using enzyme-linked immunosorbent assay. RESULTS: Chemerin and progranulin concentrations decreased following AP and PP diets. TGF-ß1 increased in AP and decreased in PP, whereas calprotectin increased in PP and decreased in AP. No statistically significant differences in the concentrations of IL-6, TNF-α, suPAR, lactoferrin and GDF-15 could be seen in either of the protein diet arms. CONCLUSIONS: These results suggest that both AP and PP diets may effectively reduce the levels of the pro-inflammatory adipokines chemerin and progranulin. The effects on the additional immune-inflammatory biomarkers seem to be more complex. CLINICAL TRIAL REGISTRY NUMBER: NCT02402985 (ww.clinicaltrials.gov).

Nutrition research in cognitive impairment/dementia, with a focus on soya and folate.

Observational studies and treatment trials investigating nutrition and cognitive function, with a focus on folate and soya and dementia, were reviewed. Data suggested that effects of folic acid based interventions may only be shown before cognitive decline is evident and/or if people are folate deficient. In older people in Indonesia, Hawai'i and China, tofu, which can contain high levels of phytoestrogens, was found to increase dementia risk. This association was not mediated by a vegetarian diet, socioeconomic status, formaldehyde, thyroid function, or loss of teeth. On the other hand, human observational and animal treatment studies suggested that tempe, a fermented soya product containing phytoestrogens and folate, reduced dementia risk and improved memory. High oestrogen levels were found to increase dementia risk in older women. However, in women with adequate serum folate, high oestrogen levels did not confer additional dementia risk and may protect ageing neurons. In conclusion, reviews seem to suggest that folic acid interventions are only effective on cognitive outcomes in people who are folate deficient and do not have cognitive impairment. Frequent consumption of tofu may have detrimental effects on memory and increase dementia risk in older East Asian people, while tempe may reduce these risks. Possibly folate in tempe offsets the potential negative effects of oestrogenic compounds on ageing neurons.

Influence of protein intake from haem and non-haem animals and plant origin on inflammatory biomarkers among apparently-healthy adults in Greece.

Intake of different types of protein may be associated with differences in biomarkers among various populations. This work investigated the influence of protein intake from haem and non-haem animals as well as protein from plants on haematological and biochemical parameters in inflammation among apparently-healthy adults living in Greece, a Mediterranean country. Four hundred and ninety apparently-healthy subjects (46 +/- 16 years, 40% men), who consecutively visited Polykliniki General Hospital for routine examinations, voluntarily agreed to participate in the study (participation rate 85%). Demographic, anthropometric and lifestyle characteristics were recorded. Participants completed a valid, semi-quantitative food frequency questionnaire. Protein intake was classified into three sources: protein from haem animals, protein from non-haem animals, and protein from plant origin. Fasting blood samples were taken from all participants; uric acid, creatinine, lipids, cystatin C, haptoglobin, haemoglobin, haematocrit, iron, ferritin, white blood cells, monocytes, platelets, and C-reactive protein were measured. Protein intake from only haem animals was associated with increased haemoglobin and haematocrit levels (p < 0.05) whereas intake of protein from non-haem animals and plant origin was not associated with the investigated haematological and biochemical markers of low-grade chronic inflammation when lifestyle factors and overall dietary habits were taken into account. Intake of protein from only haem animals seems to be consistently associated with haematological markers. The confounding role of dietary habits and lifestyle variables on the tested parameters deserves further attention in future research.

L-glutamine absorption is enhanced after ingestion of L-alanylglutamine compared with the free amino acid or wheat protein.

Differences in plasma L-glutamine (L-Gln) concentrations from ingestion of different formulations of L-Gln were examined in 8 men (26.8 ± 4.2 years old, 181.1 ± 10.9 cm, 85.8 ± 15.4 kg). Subjects reported to the laboratory on 4 separate occasions and randomly consumed 1 of 4 drinks containing 60 mg/kg of L-Gln; 89 mg/kg of Sustamine (L-alanylglutamine [AlaGln]; Kyowa Hakko Europe GmbH, Düsseldorf, Germany), which contained an equivalent L-Gln dose as consumed in L-Gln); 200 mg/kg of an enzymatically hydrolyzed wheat protein (HWP) with an L-Gln content of 31 mg/kg; or a control that consisted only of water. It was hypothesized that the AlaGln trial would increase plasma glutamine concentrations greater than the other experimental trials. Ingestion of L-Gln, AlaGln, and HWP resulted in significant increases in the plasma L-Gln concentration, peaking at 0.5, 0.5, and 0.75 hours, respectively. The corresponding mean peak increases were 179 ± 61, 284 ± 84, and 134 ± 36 µmol/L, respectively. Concentrations returned to baseline in all subjects by 2 hours after L-Gln and HWP and by 4 hours after AlaGln. Mean areas under the plasma concentration curve, calculated between 0 and 4 hours, were 127 ± 61, 284 ± 154, and 151 ± 63 µmol∙h∙L⁻¹ for L-Gln, AlaGln, and HWP, respectively. When allowance was made for the lower L-Gln dose administered as HWP, the peak plasma concentration and area under the plasma concentration curve were approximately the same as for AlaGln. The results suggest a greater transfer from the gut to plasma of L-Gln when supplied as AlaGln and possibly also as HWP compared with when the same dose was provided as the free amino acid.