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Dietary Calcium and Dairy Products Modulate Oxidative and Inflammatory Stress in Mice and Humans

md_a

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We have recently shown 1alpha,25-dihydroxycholecalciferol increased oxidative stress and inflammatory stress in vitro, whereas suppression of 1alpha,25-dihydroxycholecalciferol with dietary calcium (Ca) decreased oxidative and inflammatory stress in vivo. However, dairy products contains additional factors, such as angiotensin-converting enzyme inhibitors, which may further suppress oxidative and inflammatory stress.

Accordingly, this study was designed to study the effects of the short-term (3 wk) basal suboptimal Ca (0.4%), high-Ca (1.2% from CaCO3), and high-dairy (1.2% Ca from milk) obesigenic diets on oxidative and inflammatory stress in adipocyte fatty acid-binding protein-agouti transgenic mice. Adipose tissue reactive oxygen species (ROS) production and NADPH oxidase mRNA and plasma malondialdehyde (MDA) were reduced by the high-Ca diet (P < 0.001) compared with the basal diet and ROS and MDA were further decreased by the high-dairy diet (P < 0.001). The high-Ca and -dairy diets also resulted in suppression of adipose tissue tumor necrosis factor α and interleukin (IL)-6 mRNA (P = 0.001) compared with the basal diet, whereas an inverse pattern was noted for adiponectin and IL-15 mRNA (P = 0.002). Consequently, we conducted a follow-up evaluation of adiponectin and C-reactive protein (CRP) in archival samples from 2 previous clinical trials conducted in obese men and women. Twenty-four weeks of feeding a high-dairy eucaloric diet and hypocaloric diet resulted in an 11 (P < 0.03) and 29% (P < 0.01) decrease in CRP, respectively (post-test vs. pre-test), whereas there was no significant change in the low-dairy groups. Adiponectin decreased by 8% in subjects fed the eucaloric high-dairy diet (P = 0.003) and 18% in those fed the hypocaloric high-dairy diet (P < 0.05). These data demonstrate that dietary Ca suppresses adipose tissue oxidative and inflammatory stress.

In summary, this study provides further in vivo evidence that dietary Ca and dairy inhibit oxidative and inflammatory stress in a mouse model of diet-induced obesity and oxidative stress as well as in obese adult humans. Dietary Ca-induced suppression of circulating 1α,25-dihydroxycholecalciferol may be responsible for Ca-induced suppression of oxidative and inflammatory stress, although further effects of dairy foods on oxidative stress appear to be mediated by additional mechanisms.

Dietary Calcium and Dairy Products Modulate Oxidative and Inflammatory Stress in Mice and Humans

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For example, elevation in 1,25(OH)2D is a risk factor for kidney stones,49 and kidney stones have significant comorbidity with CD.50 However, since there is no evidence that kidney stones cause the elevation in plasma levels of 1,25(OH)2D that is associated with them,49 kidney stones are not included in Table 1.

The nine disparate conditions in Table 1 include genetic conditions (Williams syndrome, Turner syndrome, and Klinefelter syndrome),28,34,45 infectious diseases (sarcoidosis and tuberculosis),36,40 and other non-infectious diseases (hypothyroidism, primary hyperparathyroidism, lymphoma, and polycystic ovary syndrome [PCOS]).31,38,42,47

The elevated plasma levels of 1,25(OH)2D observed in these nine conditions are caused by a variety of mechanisms. In Williams syndrome, the elevated levels of 1,25(OH)2D are due to haploinsufficiency of the WSTF gene, which normally plays an important role in vitamin D homeostasis.28,51 The elevated levels of 1,25(OH)2D observed in sarcoidosis, tuberculosis, and lymphoma are caused by macrophage activation due to the underlying disease.52–54 In sarcoidosis and tuberculosis, the disease is bacterial,52,53 and in lymphoma, the disease is cancer.54

The elevated levels of 1,25(OH)2D observed in primary hyperparathyroidism are due to high levels of parathyroid hormone, which upregulates the conversion of 25(OH)D to 1,25(OH)2D
.47,55 In the case of primary hyperparathyroidism, the high levels of parathyroid hormone are generally caused by an adenoma, a non-cancerous tumor on the parathyroid gland.56

Likewise, elevated levels of parathyroid hormone are a characteristic of hypothyroidism,38 Turner syndrome,57 Klinefelter syndrome,45 and some cases of PCOS.42 As parathyroid upregulates conversion to 1,25(OH)2D as previously mentioned,47,55 it seems certain that the elevation of 1,25(OH)2D observed in these conditions is at least partly caused by the elevated levels of parathyroid hormone that are common to them. In Turner syndrome and Klinefelter syndrome, the hormone replacement therapy that is often provided to patients with these conditions also contributes to elevation in 1,25(OH)2D. Specifically, it is considered best medical practice for Turner syndrome patients to receive estrogen and for Klinefelter syndrome patients to receive testosterone,58,59 and each of these therapies increases plasma levels of 1,25(OH)2D.34,60

The effects of 1,25(OH)2D on the immune system are complex.94 One of its effects is to upregulate allergic response to foreign proteins.95 In mice, injections of 1,25(OH)2D coincident to exposure to egg albumin have been found to increase the production of immunoglobulin E and upregulate interleukin (IL) 13, a proinflammatory cytokine.95 In baby pigs, high-dose vitamin D supplementation significantly increases the number of leukocytes in blood and upregulates mucosal antimicrobial activity.96 These findings are consistent with in vitro studies on human macrophages, which also show that 1,25(OH)2D upregulates antibacterial immune activity.97,98 Separately, Leonard et al have suggested that the initiation of CD may be due to the immune system confusing the gliadin proteins in gluten with a pathogenic bacteria.99 In this light, it is conceivable that increased antibacterial immune activity in the mucosa of the small intestine caused by high plasma levels of 1,25(OH)2D may increase the risk of a dysfunctional immune reaction to gliadin in this same tissue, which may ultimately result in CD autoimmunity.

 

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