Dietary Animal to Plant Protein Ratio Is Associated with Risk Factors of Metabolic Syndrome in Participants of the AHS-2 Calibration Study

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Background: Few research studies have focused on the effects of dietary protein on metabolic syndrome and its components. Our objective was to determine the relationship between the type of dietary protein intake and animal to plant (AP) protein ratio with metabolic syndrome and its components. Methods: This population-based study had a cross sectional design and conducted on 518 participants of the Adventist Health Study 2 (AHS-2) Calibration Study. Two sets of three dietary 24-h recalls were obtained six months apart. Anthropometric measures and biochemical tests were performed in clinics. Regression calibration models were used to determine the association of type of dietary protein with metabolic syndrome and its components (raised triglyceride, raised blood pressure, reduced high-density lipoprotein cholesterol (HDL), raised fasting blood glucose and increased waist circumference). Results: The likelihood of metabolic syndrome was lower in those with higher total dietary protein and animal protein intake (p = 0.02).Total protein (β = 0.004, [95%CI: 0.002, 0.007]), animal protein intake (β = 0.004, [95%CI: 0.001, 0.007]) and AP protein intake ratio (β = 0.034, [95%CI: 0.021, 0.047]) were positively associated with waist circumference. Higher AP protein ratio was related to higher fasting blood glucose (β = 0.023, [95%CI: 0.005, 0.041]). Conclusion: Our study suggests that considering a significant amount of plant protein as a part of total dietary protein has beneficial effects on cardiometabolic risk factors.

Related collections

Most cited references 70

Record: found
Abstract: found
Article: not found

Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.

K Alberti, Robert H. Eckel, Scott M. Grundy … (2009)

A cluster of risk factors for cardiovascular disease and type 2 diabetes mellitus, which occur together more often than by chance alone, have become known as the metabolic syndrome. The risk factors include raised blood pressure, dyslipidemia (raised triglycerides and lowered high-density lipoprotein cholesterol), raised fasting glucose, and central obesity. Various diagnostic criteria have been proposed by different organizations over the past decade. Most recently, these have come from the International Diabetes Federation and the American Heart Association/National Heart, Lung, and Blood Institute. The main difference concerns the measure for central obesity, with this being an obligatory component in the International Diabetes Federation definition, lower than in the American Heart Association/National Heart, Lung, and Blood Institute criteria, and ethnic specific. The present article represents the outcome of a meeting between several major organizations in an attempt to unify criteria. It was agreed that there should not be an obligatory component, but that waist measurement would continue to be a useful preliminary screening tool. Three abnormal findings out of 5 would qualify a person for the metabolic syndrome. A single set of cut points would be used for all components except waist circumference, for which further work is required. In the interim, national or regional cut points for waist circumference can be used.

0 comments Cited 2208 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Adjustment for total energy intake in epidemiologic studies

W Willett, G R Howe, L H Kushi (1997)

In epidemiologic studies, total energy intake is often related to disease risk because of associations between physical activity or body size and the probability of disease. In theory, differences in disease incidence may also be related to metabolic efficiency and therefore to total energy intake. Because intakes of most specific nutrients, particularly macronutrients, are correlated with total energy intake, they may be noncausally associated with disease as a result of confounding by total energy intake. In addition, extraneous variation in nutrient intake resulting from variation in total energy intake that is unrelated to disease risk may weaken associations. Furthermore, individuals or populations must alter their intake of specific nutrients primarily by altering the composition of their diets rather than by changing their total energy intake, unless physical activity or body weight are changed substantially. Thus, adjustment for total energy intake is usually appropriate in epidemiologic studies to control for confounding, reduce extraneous variation, and predict the effect of dietary interventions. Failure to account for total energy intake can obscure associations between nutrient intakes and disease risk or even reverse the direction of association. Several disease-risk models and formulations of these models are available to account for energy intake in epidemiologic analyses, including adjustment of nutrient intakes for total energy intake by regression analysis and addition of total energy to a model with the nutrient density (nutrient divided by energy).

0 comments Cited 638 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance.

Christopher B. Newgard, Jie An, James Bain … (2009)

Metabolomic profiling of obese versus lean humans reveals a branched-chain amino acid (BCAA)-related metabolite signature that is suggestive of increased catabolism of BCAA and correlated with insulin resistance. To test its impact on metabolic homeostasis, we fed rats on high-fat (HF), HF with supplemented BCAA (HF/BCAA), or standard chow (SC) diets. Despite having reduced food intake and a low rate of weight gain equivalent to the SC group, HF/BCAA rats were as insulin resistant as HF rats. Pair-feeding of HF diet to match the HF/BCAA animals or BCAA addition to SC diet did not cause insulin resistance. Insulin resistance induced by HF/BCAA feeding was accompanied by chronic phosphorylation of mTOR, JNK, and IRS1Ser307 and by accumulation of multiple acylcarnitines in muscle, and it was reversed by the mTOR inhibitor, rapamycin. Our findings show that in the context of a dietary pattern that includes high fat consumption, BCAA contributes to development of obesity-associated insulin resistance.