This study aimed to utilize structural equation modeling (SEM) techniques to determine the effects of dietary calcium, protein and vitamin D on adiposity and lipidemia and to assess mediatory effects of parathyroid hormone (PTH) and 25-hydroxyvitamin D (25(OH)D) in patients with type 2 diabetes. In this cross-sectional study, a total of 150 diabetic patients (93 females and 57 males) were randomly selected. Anthropometric measures, biochemical analyses, and fat mass percent were recorded. Nutritional data were collected. SEM was performed. Based on the primary hypothesis, adiposity and lipidemia were fitted in a model. The direct effects of dietary calcium (λ = –0.165, p value = 0.002) and PTH (λ = –0.143, p value = 0.011) were significantly associated with lipidemia. There were no significant effects for dietary protein on PTH (λ = –0.270, p value = 0.057), 25(OH)D (λ = –0.071, p value = 0.613), lipidemia (λ = –0.044; p value = 0.638) or adiposity (λ = –0.009, p value = 0.949) as well as for dietary vitamin D on PTH (λ = –0.119, p value = 0.194), 25(OH)D (λ = 0.023, p value = 0.806), lipidemia (λ = 0.034, p value = 0.587) or adiposity (λ = –0.221, p value = 0.118). The correlation between calcium intake and lipidemia, and adiposity are not mediated by 25(OH)D and PTH. There were the direct effects of dietary calcium on adiposity in patients with type 2 diabetes. The model can be tested in future longitudinal and intervention studies to identify the predictors of obesity.

This study aimed to utilize structural equation modeling (SEM) techniques to determine the effects of dietary calcium, protein and vitamin D on adiposity and lipidemia and to assess mediatory effects of parathyroid hormone (PTH) and 25-hydroxyvitamin D (25(OH)D) in patients with type 2 diabetes. In this cross-sectional study, a total of 150 diabetic patients (93 females and 57 males) were randomly selected. Anthropometric measures, biochemical analyses, and fat mass percent were recorded. Nutritional data were collected. SEM was performed. Based on the primary hypothesis, adiposity and lipidemia were fitted in a model. The direct effects of dietary calcium (λ = –0.165, p value = 0.002) and PTH (λ = –0.143, p value = 0.011) were significantly associated with lipidemia. There were no significant effects for dietary protein on PTH (λ = –0.270, p value = 0.057), 25(OH)D (λ = –0.071, p value = 0.613), lipidemia (λ = –0.044; p value = 0.638) or adiposity (λ = –0.009, p value = 0.949) as well as for dietary vitamin D on PTH (λ = –0.119, p value = 0.194), 25(OH)D (λ = 0.023, p value = 0.806), lipidemia (λ = 0.034, p value = 0.587) or adiposity (λ = –0.221, p value = 0.118). The correlation between calcium intake and lipidemia, and adiposity are not mediated by 25(OH)D and PTH. There were the direct effects of dietary calcium on adiposity in patients with type 2 diabetes. The model can be tested in future longitudinal and intervention studies to identify the predictors of obesity.