This study provides evidence that pea protein (PEA), mycoprotein (MYC), and their blend (BLEND) can support postexercise myofibrillar protein synthesis rates following a bout of whole body resistance exercise. Furthermore, these data suggest that a methionine deficiency in pea may not limit its capacity to stimulate an acute increase in muscle protein synthesis (MPS).

Aim: To examine the hypothesis that there would be ethnic differences in the relationship between ectopic fat and tissue‐specific insulin resistance (IR) across a spectrum of glucose tolerance in Black African (BA) and White European (WE) men. Materials and Methods: Fifty‐three WE men (23/10/20 normal glucose tolerance [NGT]/impaired glucose tolerance [IGT]/type 2 diabetes [T2D]) and 48 BA men (20/10/18, respectively) underwent a two‐step hyperinsulinaemic‐euglycaemic clamp with infusion of D‐[6,6‐ ² H ₂ ]‐glucose and [ ² H ₅ ]‐glycerol to assess hepatic, peripheral and adipose tissue IR. Magnetic resonance imaging was used to measure subcutaneous adipose tissue, visceral adipose tissue (VAT) and intrahepatic lipid (IHL). Associations between ectopic fat and IR were assessed using linear regression models. Results: There were no differences in tissue‐specific IR between ethnic groups at any stage of glucose tolerance. VAT level was consistently lower in the BA population; NGT ( p = 0.013), IGT ( p = 0.006) and T2D ( p = 0.015). IHL was also lower in the BA compared with the WE men ( p = 0.013). VAT and IHL levels were significantly associated with hepatic IR in the BA population ( p = 0.001) and with peripheral IR in the WE population ( p = 0.027). Conclusions: The present study suggests that BA and WE men exhibit the same degree of IR across a glucose tolerance continuum, but with lower VAT and IHL levels in the BA population, suggesting that IR may be driven by a mechanism other than increased ectopic fat accumulation in BA men.

Background: High‐protein diets have been recognized as a potential strategy in the nutritional management of type 2 diabetes (T2D). Mycoprotein is a high‐fibre, high‐protein food ingredient previously shown to improve acute glycaemic control. We determined whether incorporating mycoprotein into a high‐protein vegan diet would improve glycaemic control to a greater extent than an isonitrogenous omnivorous diet in people with T2D. Methods: Seventeen adults ( f = 5, age = 58.3 ± 8.3 years, BMI = 32.9 ± 4.7 kg∙m ⁻² , HbA1c = 60 ± 15 mmol∙mol ⁻¹ ) with T2D were randomly allocated to a 5‐week eucaloric high‐protein (30% energy from protein) diet, either an omnivorous diet (OMNI; 70% protein from omnivorous sources) or an isonitrogenous, mycoprotein‐rich, vegan diet (VEG; 50% protein from mycoprotein). Glycaemic control was assessed using a two‐step hyperinsulinaemic‐euglycaemic clamp (HEC) with D‐[6,6‐ ² H ₂ ] glucose infusion, a mixed‐meal tolerance test (MMTT) and continuous glucose monitoring. Results: The rate of glucose disappearance (RdT), glucose disposal rate and endogenous glucose production, as well as postprandial time‐course of blood glucose, serum insulin and C‐peptide were assessed during the HEC and MMTT, respectively. Both groups had improved peripheral insulin sensitivity (intervention effect, p = 0.006; increased RdT/Insulin of 1.0 ± 0.6 and 1.0 ± 0.3 mg kg ⁻¹ min ⁻¹ in OMNI and VEG, respectively), HbA1c (intervention; p = 0.001) and glycaemic variability (intervention; p = 0.040; increased time in‐range of 11.8 ± 9.3% and 23.3 ± 12.9% in OMNI and VEG). There were no improvements in hepatic insulin sensitivity or in postprandial blood glucose and serum C‐peptide ( p > 0.05) during the MMTT. Conclusions: High‐protein diets, whether predicated on vegan or omnivorous proteins, can improve glycaemic control by increasing peripheral insulin sensitivity in people with T2D.

Background: Mycoprotein is a high-fibre food previously shown to reduce postprandial glucose concentrations when ingested within a mixed-meal. We applied a dual stable isotope tracer approach to determine whether this is due to a reduced rate of appearance of glucose, in participants of ranging BMI. Methods: Twenty-four adults (F = 8, BMI 30 ± 6 kg·m⁻²) attended 2 trials in a double-blind, randomised, cross-over design. Participants ingested two energy and macronutrient matched milk-based drinks (enriched with 1000 mg [U-¹³C₆] glucose in a subset of 12 participants), containing 50 g glucose and either 0 (CON) or 20 g (MYC) mycoprotein. A primed continuous intravenous infusion of D-[6,6-²H₂] glucose determined plasma glucose kinetics over 6 h. Postprandial time-course, and AUC, of glucose and insulin concentration, rate of disappearance (RdT) and appearance of exogenous (RaEx), endogenous (EGP), and total (RaT) plasma glucose were assessed using two- and one-way ANOVA. Results: Drink ingestion increased blood glucose and serum insulin concentrations (P < 0.05) and were comparable between conditions (P > 0.05). Both RaT and RdT were higher with MYC compared with CON over 6 h (mean 6 h glucose appearance and disappearance increased by 5 and 9%, respectively, P < 0.05). RaEx was not affected by MYC ingestion over 6 h (P > 0.05). The mean contribution of EGP to total glucose appearance was 15% greater with MYC, with a trend towards significance (P = 0.05). There was no relationship between BMI and the response to MYC ingestion for any of the variables (P < 0.05). Conclusion: The ingestion of mycoprotein within a mixed-meal impacted postprandial glucose kinetics, but not blood glucose or serum insulin concentrations, in individuals of ranging BMI. Clinical trial registry number and website: This trial was registered at clinicaltrials.gov as NCT04084639 and can be accessed at https://clinicaltrials.gov/ct2/show/NCT04084639.

Aims/hypothesis: People of Black African (BA) ancestry are disproportionately affected by type 2 diabetes when compared with people of White European (WE) descent, despite lower levels of ectopic fat. Impaired beta cell function is a key pathophysiological feature of type 2 diabetes. It remains to be determined whether an associative relationship exists between intrapancreatic lipid (IPL) accumulation and beta cell function, and whether this differs by ethnicity. Methods: Fifty-three BA (23 normal glucose tolerance, 11 impaired glucose tolerance and 19 type 2 diabetes) and 51 WE (23/13/15) men underwent a hyperglycaemic clamp and mixed-meal tolerance test to assess insulin secretion and beta cell function, a hyperinsulinaemic–euglycaemic clamp to measure insulin sensitivity and Dixon MRI to determine IPL. Associations between IPL and beta cell function were assessed using linear regression. Results: IPL was lower in BA compared with WE men (mean ± SD; 7.6 ± 2.6% vs 8.8 ± 3.7%, p=0.038), but after adjustment for waist circumference this ethnic difference no longer occurred (p=0.278). BA men with type 2 diabetes had lower total insulin secretion response to the mixed-meal (p=0.001) and hyperglycaemic clamp (p=0.002), but no ethnic differences were observed in the disposition index within glucose tolerance groups. IPL was inversely associated with beta cell function in the WE but not the BA men, but after adjustment for confounders these associations were not significant. Conclusions/interpretation: Ethnic differences were apparent as beta cell function was inversely associated with IPL in the WE, but not BA, men. However, in both ethnic groups, this relationship appears secondary to other factors, such as adiposity, in the pathogenesis of type 2 diabetes. Graphical

Postprandial TAG is lower in Black African-Caribbean men than in White European men, and this is likely driven by lower meal-derived VLDL-TAG in Black African-Caribbean men. This observation could suggest that fatty acid trafficking may be a less important determinant of cardiometabolic risk in Black Africans than in White European men.