Dampened Muscle mTORC1 Response Following Ingestion of High-Quality Plant-Based Protein and Insect Protein Compared to Whey

Increased amino acid availability acutely stimulates protein synthesis partially via activation of mechanistic target of rapamycin complex 1 (mTORC1). Plant-and insect-based protein sources matched for total protein and/or leucine to animal proteins induce a lower postprandial rise in amino acids, but their effects on mTOR activation in muscle are unknown. C57BL/6J mice were gavaged with different protein solutions: whey, a pea–rice protein mix matched for total protein or leucine content to whey, worm protein matched for total protein, or saline. Blood was drawn 30, 60, 105 and 150 min after gavage and muscle samples were harvested 60 min and 150 min after gavage to measure key components of the mTORC1 pathway. Ingestion of plant-based proteins induced a lower rise in blood leucine compared to whey, which coincided with a dampened mTORC1 activation, both acutely and 150 min after administration. Matching total leucine content to whey did not rescue the reduced rise in plasma amino acids, nor the lower increase in mTORC1 compared to whey. Insect protein elicits a similar activation of downstream mTORC1 kinases as plant-based proteins, despite lower postprandial aminoacidemia. The mTORC1 response following ingestion of high-quality plant-based and insect proteins is dampened compared to whey in mouse skeletal muscle.     

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Monoclonal gammopathy after intense induction immunosuppression in renal transplant patients

OBJECTIVES.: Incidence and risk factors of post-transplant monoclonal gammopathywere studied in renal transplant patients who received theirgrafts between 1982 and 1992 (n=390 grafts). Immunoelectrophoresiswas performed at annual intervals after transplantation. RESULTS.: Forty-six cases of clonal gammopathy were detected: 35 monoclonal,11 bi- or triclonal, with a predominance of IgG and K light-chainsubtypes (IgG, 39; IgA, 3; IgM, 4; K, 35; , 19). Gammopathywas transient in 17 patients (37%). The 5-year cumulative incidenceof gammopathy was 10.7%, much higher than expected for a groupof similar age from the general population. Thirty of the 46gammopathies appeared within the first 2 years of transplantation.Gammopathy never progressed to multiple myeloma during follow-up(median 1 year; (range 0–10)); one patient subsequentlydeveloped Kaposi sarcoma. The 2-year incidence of gammopathywas much higher in patients transplanted in 1989–1991(23/142) than in 1982–1988 (7/248) (P<0.0001). Thiscoincided with the use of quadruple induction immunosuppression(cyclosporin A+azathioprine+prednisone plus either ATG-Fresenius(ATG-F) or OKT3) since 1989. The risk for acquiring gammopathywithin 2 years of transplantation was 14.7% (95% CI 9.2, 20.3%)in patients receiving quadruple induction therapy, but only3.0% (CI 1.2, 6.1%) without such therapy (P<0.0001). Therisk for patients receiving quadruple immunosuppression withOKT3 was 24.5%, significantly greater than with ATG-F (11.8%,P<0.05). Discriminant analysis revealed that the type ofimmunosuppression, but not age or year of transplantation, wereindependent risk factors for gammopathy. CONCLUSIONS.: Monoclonal gammopathy frequently occurs after renal transplantation.Risks are higher for patients receiving quadruple inductionimmunosuppression, particularly if it includes OKT3. Follow-upof these patients is warranted for the early detection of malignanttransformation.     

In vitro and in vivo down-regulation of human plateletα 2-adrenoceptors by clonidine

Summary The effect of clonidine on the number of ₂-adrenoceptors in human platelet membranes, determined by³H-yohimbine binding, was investigatedin vitro andin vivo. Incubation of platelet membranes with clonidine (1–100 µM) for 16 h at 25 °C led to a concentration-dependent decrease in the number of³H-yohimbine binding sites of 10–25%; the affinity of³H-yohimbine to the sites was not changed (K_D approximately 3–4 nM). In such desensitized membranes, inhibition of³H-yohimbine binding by clonidine resulted in steep, monophasic displacement curves, which in comparison to the curves from control membranes (IC₅₀ for clonidine 90 nM), were shifted to the right (IC₅₀: 321 nM) and were not affected by 10^–4M guanosine-5-triphosphate (GTP).Treatment of 3 hypertensive patients with clonidine (3×150 µg/d for 7 days) reduced blood pressure and heart rate. Simultaneously, both³H-yohimbine binding sites on platelet membranes and plasma catecholamine levels decreased within three days and remained at a reduced level during treatment. After abrupt cessation of clonidine treatment, blood pressure, heart rate and plasma catecholamines rapidly increased, reaching values after two days similar to or higher than those before treatment.³H-yohimbine binding sites, however, initially decreased further before returning to control values. In platelet membranes derived from hypertensive patients treated with clonidine for at least three weeks, GTP (10^–4M) had no influence on inhibition of³H-yohimbine binding by (—)-adrenaline and clonidine. It is concluded that clonidine desensitizes ₂-adrenoceptors in human platelet membranesin vitro andin vivo. An important step in the desensitization process is the uncoupling of receptor occupancy by agonists and adenylate cyclase activity, as indicated by loss of the regulatory activity of GTP on desensitized membranes. The clonidine withdrawal syndrome may be caused by enhanced release of endogenous catecholamines not adequately regulated by presynaptic ₂-adrenoceptors, which have become subsensitive after chronic clonidine treatment.     

Immunogenicity and reactogenicity of a Haemophilus influenzae type b tetanus conjugate vaccine when administered separately or mixed with concomitant diphtheria-tetanus-toxoid and acellular pertussis vaccine for primary and for booster immunizations

With an increasing number of new vaccines available for routine childhood immunization, combination vaccines are needed in order to maintain or achieve a high compliance with recommended immunization programmes. In a prospective, randomized, comparative, multi-centre study, 822 healthy infants were enrolled to receive three doses of either a candidate or a commercially available Haemophilus influenzae type b (Hib) vaccine concomitantly with diphtheria-, tetanus- acellular pertussis (DTaP) vaccine. Study subjects were randomly allocated to one of the following groups: (1) separate, or (2) mixed injection of DTaP and candidate Hib vaccine, or (3) separate injection of DTaP and commercial Hib vaccine. One year later the first 189 study subjects received either separate or mixed injections of the same Hib and DTaP vaccines as booster doses. Evaluation of reactogenicity was based on diary cards completed by parents. Immunogenicity was documented by measuring IgG antibody concentrations in serum samples taken before and 4 weeks after primary and booster vaccination. No serious adverse events occurred and most local and systemic reactions were mild to moderate. Booster doses were more reactogenic than primary doses with all groups. Antibody concentrations against pertussis antigens were similar to those seen with DTaP alone. All but one subject had protective antibody concentrations against diphtheria and tetanus. Primary immune response to the Hib vaccine was significantly lower in the group receiving the mixed Hib-DTaP vaccine, however, ≥95% of vaccinees had anti-Hib antibody concentrations ≥0.15 μg/ml and there was a marked booster response (>100-fold) in all groups. Conclusions Mixing DTaP and Hib vaccines for primary immunization caused a decrease in anti-Hib antibody response, although after primary immunization as after booster doses, all subjects showed antibody concentrations considered to be protective for invasive Hib disease. Mixing of the vaccines did not result in increased reactogenicity. Received: 13 June 1997 / Accepted in revised form: 4 September 1997