Iron and Vitamin D/Calcium Deficiency after Gastric Bypass: Mechanisms Involved and Strategies to Improve Oral Supplement Disposition

Mangan, Aisling; Roux, Carel W. le; Miller, Nana Gletsu; Docherty, Neil G.

doi:10.2174/1389200219666181026160242

Cited by 18 publications

(17 citation statements)

References 87 publications

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“…Another limitation of this study is that the effect of the potentially altered 25-hydroxylation on vitamin D status cannot be well-studied in this model, as vitamin D deficiency is a common consequence of gastric bypass operation because of impaired gastric absorption. (34) It is currently unclear whether obesity-induced CYP2R1 repression in adipose tissue could contribute to the reduced plasma 25-OH-levels. Interestingly, according to the human tissue atlas, 20 CYP2R1 appears to be expressed rather ubiquitously in most tissues, and the liver expression is not particularly high among human tissues ( Supplementary Fig.…”

Section: Discussionmentioning

confidence: 99%

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Obesity Represses CYP2R1, the Vitamin D 25‐Hydroxylase, in the Liver and Extrahepatic Tissues

et al. 2020

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Low plasma level of 25-hydroxyvitamin D (25-OH-D), namely vitamin D deficiency, is associated with obesity and weight loss improves 25-OH-D status. However, the mechanism behind obesity-induced vitamin D deficiency remains unclear. Here, we report that obesity suppresses the expression of cytochrome P450 (CYP) 2R1, the main vitamin D 25-hydroxylase, in both mice and humans. In humans, weight loss induced by gastric bypass surgery increased the expression of CYP2R1 in the s.c. adipose tissue suggesting recovery after the obesity-induced suppression. At the same time, CYP27B1, the vitamin D 1α-hydroxylase, was repressed by the weight loss. In a mouse (C57BL/6N) model of diet-induced obesity, the plasma 25-OH-D was decreased. In accordance, the CYP2R1 expression was strongly repressed in the liver. Moreover, obesity repressed the expression of CYP2R1 in several extrahepatic tissues, the kidney, brown adipose tissue, and testis, but not in the white adipose tissue. Obesity had a similar effect in both male and female mice. In mice, obesity repressed expression of the vitamin D receptor in brown adipose tissue. Obesity also upregulated the expression of the vitamin D receptor and CYP24A1 in the s.c. adipose tissue of a subset of mice; however, no effect was observed in the human s.c. adipose tissue. In summary, we show that obesity affects CYP2R1 expression both in the mouse and human tissues. We suggest that in mouse the CYP2R1 repression in the liver plays an important role in obesity-induced vitamin D deficiency. Currently, it is unclear whether the CYP2R1 downregulation in extrahepatic tissues could contribute to the obesity-induced low plasma 25-OH-D, however, this phenomenon may affect at least the local 25-OH-D concentrations.

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Section: Discussionmentioning

confidence: 99%

“…Another limitation of this study is that the effect of the potentially altered 25‐hydroxylation on vitamin D status cannot be well‐studied in this model, as vitamin D deficiency is a common consequence of gastric bypass operation because of impaired gastric absorption. ( 34 )…”

Section: Discussionmentioning

confidence: 99%

Obesity Represses CYP2R1, the Vitamin D 25‐Hydroxylase, in the Liver and Extrahepatic Tissues

et al. 2020

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“…In a 2019 questionnaire-based survey on 533 BS patients, Mahawar et al showed that slightly over half of the respondents reported non-adherence to micronutrient supplementation [107]. The main micronutrient deficiencies reported after RYGB and VSG include vitamin B 12 , folic acid, iron, thiamine (vitamin B 1 ), vitamin D, and calcium [108][109][110][111][112]. Other reports on nutritional deficiencies after weight loss surgery, particularly following mixed bariatric procedures, are for fat liposoluble soluble vitamins, namely, vitamin A [113], vitamin E [114], and vitamin K [115], as well as for copper [116], zinc, and selenium [117,118].…”

Section: Pathogenesis Of Micronutrient Deficiencies After Bsmentioning

confidence: 99%

Bariatric Surgery in Obesity: Effects on Gut Microbiota and Micronutrient Status

et al. 2020

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Obesity is associated with reduced gut microbial diversity and a high rate of micronutrient deficiency. Bariatric surgery, the therapy of choice for severe obesity, produces sustained weight loss and improvements in obesity-related comorbidities. Also, it significantly alters the gut microbiota (GM) composition and function, which might have an important impact on the micronutrient status as GM is able to synthesize certain vitamins, such as riboflavin, folate, B12, or vitamin K2. However, recent data have reported that GM is not fully restored after bariatric surgery; therefore, manipulation of GM through probiotics represents a promising therapeutic approach in bariatric patients. In this review, we discuss the latest evidence concerning the relationship between obesity, GM and micronutrients, the impact of bariatric surgery on GM in relation with micronutrients equilibrium, and the importance of the probiotics’ supplementation in obese patients submitted to surgical treatment.

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“…The impact of modification of the length of the standard RYGB alimentary limb should be investigated to determine if a shorter limb length can achieve comparable metabolic control and weight-independent renoprotective benefits while minimising hyperoxaluria risk to improve net renal outcomes. Additionally, nutritional deficiencies in iron, calcium, and vitamin D after metabolic surgery may exacerbate anaemia and mineral bone disease as complications of CKD (130). Oxalosis as a consequence of enteric hyperoxaluria may also result in erythopoeitin-stimulating agent resistant anaemia (131).…”

Section: Future Directionsmentioning

confidence: 99%

Metabolic Surgery to Treat Obesity in Diabetic Kidney Disease, Chronic Kidney Disease, and End-Stage Kidney Disease; What Are the Unanswered Questions?

et al. 2020

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Obesity is a major factor in contemporary clinical practice in nephrology. Obesity accelerates the progression of both diabetic and non-diabetic chronic kidney disease and, in renal transplantation, both recipient and donor obesity increase the risk of allograft complications. Obesity is thus a major driver of renal disease progression and a barrier to deceased and living donor kidney transplantation. Large observational studies have highlighted that metabolic surgery reduces the incidence of albuminuria, slows chronic kidney disease progression, and reduces the incidence of end-stage kidney disease over extended follow-up in people with and without type 2 diabetes. The surgical treatment of obesity and its metabolic sequelae has therefore the potential to improve management of diabetic and non-diabetic chronic kidney disease and aid in the slowing of renal decline toward end-stage kidney disease. In the context of patients with end-stage kidney disease, although complications of metabolic surgery are higher, absolute event rates are low and it remains a safe intervention in this population. Pre-transplant metabolic surgery increases access to kidney transplantation in people with obesity and end-stage kidney disease. Metabolic surgery also improves management of metabolic complications post-kidney transplantation, including new-onset diabetes. Procedure selection may be critical to mitigate the risks of oxalate nephropathy and disruption to immunosuppressant pharmacokinetics. Metabolic surgery may also have a role in the treatment of donor obesity, which could increase the living kidney donor pool with potential downstream impact on kidney paired exchange programmes. The present paper provides a comprehensive coverage of the literature concerning renal outcomes in clinical studies of metabolic surgery and integrates findings from relevant mechanistic pre-clinical studies. In so doing the key unanswered questions for the field are brought to the fore for discussion.

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Iron and Vitamin D/Calcium Deficiency after Gastric Bypass: Mechanisms Involved and Strategies to Improve Oral Supplement Disposition

Cited by 18 publications

References 87 publications

Obesity Represses CYP2R1, the Vitamin D 25‐Hydroxylase, in the Liver and Extrahepatic Tissues

Obesity Represses CYP2R1, the Vitamin D 25‐Hydroxylase, in the Liver and Extrahepatic Tissues

Bariatric Surgery in Obesity: Effects on Gut Microbiota and Micronutrient Status

Metabolic Surgery to Treat Obesity in Diabetic Kidney Disease, Chronic Kidney Disease, and End-Stage Kidney Disease; What Are the Unanswered Questions?

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