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Protein ingestion concurrently stimulates euglycemic glucagon and insulin secretion, a response that is particularly robust with rapidly absorbing proteins. Previously, we have shown that ingestion of repeated doses of rapidly absorbing whey protein equally stimulated endogenous glucose production (EGP) and glucose disposal (Rd), thus explaining the preservation of euglycemia. Here, we aimed to determine if a smaller single dose of whey could elicit a large enough glucagon and insulin response to stimulate glucose flux. Therefore, in normoglycemic young adult males (n = 10; age ~26; BMI ~25), using [6,6-²H2] glucose tracing and quantitative targeted metabolite profiling, we determined the metabolic response to a single 25 g "standard" dose of whey protein. Whey protein ingestion did not alter glycemia, but increased circulating glucagon (peak 4-fold basal), insulin (peak 6-fold basal), amino acids, and urea while also reducing free fatty acid (FFA) and glycerol concentrations. Interestingly, the postprandial insulin response was driven by both a stimulation of insulin secretion and marked reduction in hepatic insulin clearance. Whey protein ingestion resulted in a modest stimulation of EGP and Rd, both peaking at ~20% above baseline 1 h after protein ingestion. These findings demonstrate that the ingestion of a single standard serving of whey protein can induce a euglycemic glucagon and insulin response that stimulates glucose flux. We speculate on a theory that could potentially explain how glucagon and insulin synergistically provide hardwired control of nitrogen and glucose homeostasis. NEW & NOTEWORTHY Protein ingestion concurrently stimulates glucagon and insulin secretion. Here we show that in normoglycemic males, ingestion of a single "standard" 25 g serving of rapidly absorbing whey protein drives a sufficiently large glucagon and insulin response, such that it simultaneously increases endogenous glucose production and glucose disposal. We speculate on a novel theory that could potentially explain how the antagonistic/synergistic actions of glucagon and insulin simultaneously provide tight control of glucose and nitrogen homeostasis. [ABSTRACT FROM AUTHOR]

Aim: The primary aim of this study was to investigate whether ascorbic acid (AA) supplementation improves postprandial glucose responses under free‐living conditions in individuals with type 2 diabetes. A secondary aim was to investigate the effect of AA supplementation on blood pressure. Materials and methods: A total of 31 individuals with type 2 diabetes (26 males and 5 females; aged 61.8 ± 6.8 years; duration of diabetes, 5.6 ± 4.6 years; HbA1c, 7.6% ± 0.7% [mean ± SD]) were enrolled in a randomized cross‐over study involving 4 months of supplementation with oral AA (2 × 500 mg/d) or placebo. Participants wore continuous glucose monitors for 48 hours and consumed standardized meals pre‐ and post‐supplementation. Measurements included postprandial glucose incremental areas under the curve (iAUC), duration of day in hyper‐ and hypo‐glycaemia status, average 24‐hour and daily postprandial glucose concentrations, HbA1c, insulin, blood pressure (BP) and oxidative stress (F2‐isoprostanes). Results: Following AA supplementation, significant decreases were observed in daily postprandial glucose iAUC (−36%), in duration of day with hyperglycaemia (−2.8 h/d) and postprandial hyperglycaemia (−1.7 h/d), in average 24‐hour glucose (−0.8 mmol/L) and daily postprandial glucose (−1.1 mmol/L) concentrations, in systolic (−7 mm Hg) and diastolic (−5 mm Hg) blood pressures and in a specific fraction of free plasma F2‐isoprostanes (−47 pg/mL) as compared to placebo. Conclusions: Individuals with type 2 diabetes experienced improved postprandial and 24‐hour glycaemia and decreased BP after 4 months of AA supplementation as compared to placebo. These findings offer evidence for the proposed use of AA as an adjunct therapy to improve glycaemic and BP control in individuals with type 2 diabetes. [ABSTRACT FROM AUTHOR]

High Na intake and chronically elevated cortisol levels are independently associated with the development of chronic diseases. In adults, high Na intake is associated with high levels of urinary cortisol. We aimed to determine the association between urinary Na and K and urinary cortisol in a cross-sectional sample of Australian schoolchildren and their mothers. Participants were a sample of Australian children (n 120) and their mothers (n 100) recruited through primary schools. We assessed Na, K, free cortisol and cortisol metabolites in one 24 h urine collection. Associations between 24 h urinary electrolytes and 24 h urinary cortisol were assessed using multilevel mixed-effects linear regression models. In children, urinary Na was positively associated with urinary free cortisol (β=0·31, 95 % CI 0·19, 0·44) and urinary cortisol metabolites (β=0·006, 95 % CI 0·002, 0·010). Positive associations were also observed between urinary K and urinary free cortisol (β=0·65, 95 % CI 0·23, 1·07) and urinary cortisol metabolites (β=0·02, 95 % CI 0·03, 0·031). In mothers, urinary Na was positively associated with urinary free cortisol (β=0·23, 95 % CI 0·01, 0·50) and urinary cortisol metabolites (β=0·008, 95 % CI 0·0007, 0·016). Our findings show that daily Na and K intake were positively associated with cortisol production in children and their mothers. Investigation of the mechanisms involved and the potential impact of Na reduction on cortisol levels in these populations is warranted.