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Background: Epidemiologic studies have linked high consumption of red and processed meat with risk of developing type 2 diabetes, whereas high dairy consumption has been associated with decreased risk, but interventions have been limited. Objective: We compared the effects on insulin sensitivity of consuming a diet high in lean red meat with minimal dairy, a diet high in primarily low-fat dairy (from milk, yogurt, or custard) with no red meat, and a control diet that contained neither red meat nor dairy. Design: A randomized crossover study was undertaken with 47 overweight and obese men and women divided into 2 groups as follows: those with normal glucose tolerance and those with impaired fasting glucose or impaired glucose tolerance. Participants followed the 3 weight-stable dietary interventions for 4 wk with glucose, insulin, and C-peptide measured by using oral-glucose-tolerance tests at the end of each diet. Results: Fasting insulin was significantly higher after the dairy diet than after the red meat diet (P , 0.01) with no change in fasting glucose resulting in a decrease in insulin sensitivity after the highdairy diet (P , 0.05) as assessed by homeostasis model assessment of insulin resistance (HOMA-IR). A significant interaction between diet and sex was observed such that, in women alone, HOMA-IR was significantly lower after the red meat diet than after the dairy diet (1.33 6 0.8 compared with 1.71 6 0.8, respectively; P , 0.01). Insulin sensitivity calculated by using the Matsuda method was 14.7% lower in women after the dairy diet than after the red meat diet (P , 0.01) with no difference between diets in men. C-peptide was not different between diets. Conclusion: In contrast to some epidemiologic findings, these results suggest that high consumption of dairy reduces insulin sensitivity compared with a diet high in lean red meat in overweight and obese subjects, some of whom had glucose intolerance. This trial was registered at the Australian New Zealand Clinical Trials Registry as ACTRN12613000441718.

There is a body of evidence linking inflammation, altered lipid metabolism, and insulin resistance. Our previous research found that insulin sensitivity decreased after a four-week diet high in dairy compared to a control diet and to one high in red meat. Our aim was to determine whether a relationship exists between changes in insulin sensitivity and inflammatory biomarkers, or with lipid species. Fasting Tumor Necrosis Factor alpha (TNF-α), Tumor Necrosis Factor Receptor II (sTNF-RII), C-reactive protein (CRP), and lipids were measured at the end of each diet. TNF-α and the ratio TNF-α/sTNF-RII were not different between diets and TNF-α, sTNF-RII, or the ratio TNF-α/sTNF-RII showed no association with homeostasis model assessment-estimated insulin resistance (HOMA-IR). A number of phosphatidylethanolamine (PE) and phosphatidylinositol (PI) species differed between dairy and red meat and dairy and control diets, as did many phosphatidylcholine (PC) species and cholesteryl ester (CE) 14:0, CE15:0, lysophosphatidylcholine (LPC) 14:0, and LPC15:0. None had a significant relationship (p = 0.001 or better) with log homeostasis model assessment-estimated insulin resistance (HOMA-IR), although LPC14:0 had the strongest relationship (p = 0.004) and may be the main mediator of the effect of dairy on insulin sensitivity. LPC14:0 and the whole LPC class were correlated with CRP. The correlations between dietary change and the minor plasma phospholipids PI32:1 and PE32:1 are novel and may reflect significant changes in membrane composition. Inflammatory markers were not altered by changes in protein source while the correlation of LPC with CRP confirms a relationship between changes in lipid profile and inflammation.

Background: In contrast with some epidemiologic evidence, our previous research showed that a 4-wk diet that was high in low-fat dairy reduced insulin sensitivity compared with the effect of a diet that was high in red meat. Objective: We investigated whether a dairy meal would produce a greater insulin response than a carbohydrate-matched red meat meal would, which might account for the change in insulin sensitivity. Design: One meal contained lean red meat, bread, and orange juice, and the other meal contained skim milk, low-fat yogurt, cheese, and bread. Meals were isoenergetic, equal in macronutrient profile, and consumed 1 wk apart. Glucose, insulin, and triglycerides were measured before and 30, 60, 90, 120, 150, and 180 min after meal consumption. Differences between meals were tested with the use of a repeated-measures ANOVA and paired sample t tests. Results: Nineteen men and 24 women [mean 6 SD age: 50.8 6 16.0 y; body mass index (in kg/m 2 ): 30.0 6 3.5] completed the study. Twenty-two participants had normal glucose tolerance, and 21 participants had impaired fasting glucose or impaired glucose tolerance. The red meat meal resulted in a higher glucose response at 30 min after consumption (P , 0.001); however, the glucose total AUC was not different between meals (P = NS). The mean 6 SEM incremental AUC (iAUC) for glucose was significantly higher after the dairy meal than after the red meat meal (2.23 6 0.49 compared with 0.88 6 0.57 mmol/L $ 3 h, respectively; P = 0.004). The insulin total AUC and iAUC were not different between meals (iAUC: 159.65 6 20.0 mU/L $ 3 h for red meat compared with 167.49 6 24.1 mU/L $ 3 h for dairy; P = NS). Conclusions: Lean red meat and low-fat dairy produced a similar glycemic response. The higher glucose response 30 min after consumption of the red meat meal was likely attributable to differences in the glycemic load between orange juice and milk and yogurt. An insulinotropic effect of dairy was not observed. This trial was registered at www.anzctr.org.au as ACTRN12615000164594.Am J Clin Nutr 2016;103:71-6.