We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (-47%), the Apo B/Apo A-1 ratio (-16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.

Abnormal distribution of plasma fatty acids and increased inflammation are prominent features of metabolic syndrome. We tested whether these components of metabolic syndrome, like dyslipidemia and glycemia, are responsive to carbohydrate restriction. Overweight men and women with atherogenic dyslipidemia consumed ad libitum diets very low in carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks. In comparison to the LFD, the VLCKD resulted in an increased proportion of serum total n-6 PUFA, mainly attributed to a marked increase in arachidonate (20:4n-6), while its biosynthetic metabolic intermediates were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid ratio also increased sharply. Total saturated fatty acids and 16:1n-7 were consistently decreased following the VLCKD. Both diets significantly decreased the concentration of several serum inflammatory markers, but there was an overall greater anti-inflammatory effect associated with the VLCKD, as evidenced by greater decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.

Crossbred pigs (n = 512) with an average initial BW of 22.1 +/- 0.54 kg were used to evaluate growth performance, carcass characteristics, and pork fat quality of grower-finisher pigs fed corn-soybean meal diets containing increasing content of distillers dried grains with solubles (DDGS). One of 4 dietary treatments was randomly assigned to each pen within sex. Dietary treatment and sex were the main factors in a 3-phase feeding program (BW = 22 to 53 kg, 53 to 85 kg, and 85 to 115 kg). Dietary treatments consisted of a corn-soybean meal control, or a corn-soybean meal diet containing 10, 20, or 30% DDGS. Overall, increasing the dietary DDGS content had no effect on ADG (P = 0.74), but ADFI was linearly reduced and G:F was linearly increased (P < 0.01). Dressing percentage, LM marbling and firmness, and belly firmness were linearly reduced (P < 0.01), but percentage of fat-free lean was linearly increased (P < 0.05) with increasing dietary DDGS. Subjective LM color score (P = 0.65), drip loss (P = 0.37), and ultimate pH of LM (P = 0.21) were not influenced by dietary DDGS. Japanese color scores for backfat (P = 0.41) and belly fat (P = 0.85) were similar among dietary treatments (P = 0.41). Feeding an increasing content of DDGS linearly increased (P < 0.05) PUFA concentration, particularly linoleic acid (C18:2), in belly fat, backfat, and LM intramuscular fat, but the increase in LM intramuscular fat was smaller in magnitude (P < 0.05) than in backfat and belly fat. Pigs fed an increasing content of DDGS had a linear increase (P < 0.05) in the iodine value of backfat, belly fat, and LM intramuscular fat of 58.4 to 72.4, 61.5 to 72.3, and 54.8 to 57.7, respectively. Oxidation of LM intramuscular fat measured on d 0, 14, 21, and 28 of storage was not affected by dietary treatment. Taste tests for LM showed no effects of diet on flavor, off-flavor (P = 0.36), tenderness (P = 0.66), juiciness (P = 0.58), and overall acceptability (P = 0.52) scores. Similarly, bacon flavor (P = 0.88), off-flavor, crispiness, and overall liking scores were not affected by increasing dietary DDGS, but bacon fattiness (P < 0.01) and tenderness (P < 0.05) scores were linearly reduced. These results showed no negative effects on growth performance or dressing percentage when growing-finishing pigs were fed diets containing up to 30% DDGS, but fat quality may not meet the standards of all pork processors when feeding diets containing more than 20% DDGS.