ArticleBiochemical and biophysical research communications2011
Genetic induction of phosphate toxicity significantly reduces the survival of hypercholesterolemic obese mice.
Article in Biochemical and biophysical research communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Can salivary phosphate levels be an early biomarker to monitor the evolvement of obesity?Contributions to nephrology · 2013Trial
- Integrated omics reveal the effects of vitamin D deficiency on gut microbiota and plasma metabolism in experimental autoimmune uveitis.Journal of neuroinflammation · 2026Article
- Specialty grand challenge: existing issues and emerging frontiers in renal endocrinology.Frontiers in endocrinology · 2025Article
- Obesity, Diabetes Mellitus, and Vascular Impediment as Consequences of Excess Processed Food Consumption.Cureus · 2022Review
- Salivary phosphate as a biomarker for human diseases.FASEB bioAdvances · 2022Article
- Phosphate Burden and Inflammation.Advances in experimental medicine and biology · 2022Article
- Dietary phosphate toxicity: an emerging global health concern.Histochemistry and cell biology · 2018Review
- The role of Klotho in energy metabolism.Nature reviews. Endocrinology · 2012Review
- Can features of phosphate toxicity appear in normophosphatemia?Journal of bone and mineral metabolism · 2012Review
- Lack of awareness among future medical professionals about the risk of consuming hidden phosphate-containing processed food and drinks.PloS one · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe adverse effects of metabolic disorders in obesity have been extensively studied; however, the pathologic effects of hyperphosphatemia or phosphate toxicity in obesity have not been studied in similar depth and detail, chiefly because such an association is thought to be uncommon. Studies have established that the incidence of obesity-associated nephropathy is increasing. Because hyperphosphatemia is a major consequence of renal impairment, this study determines the in vivo effects of hyperphosphatemia in obesity. METHODS AND
resultsWe genetically induced hyperphosphatemia in leptin-deficient obese (ob/ob) mice by generating ob/ob and klotho double knockout [ob/ob-klotho(-/-)] mice. As a control, we made ob/ob mice with hypophosphatemia by generating ob/ob and 1-alpha hydroxylase double knockout [ob/ob-1α(OH)ase(-/-)] mice. Compared to the wild-type mice, all three obese background mice, namely ob/ob, ob/ob-klotho(-/-), and ob/ob-1α(OH)ase(-/-) mice developed hypercholesterolemia. In addition, the hyperphosphatemic, ob/ob-klotho(-/-) genetic background induced generalized tissue atrophy and widespread soft-tissue and vascular calcifications, which led to a shorter lifespan; no such changes were observed in the hypophosphatemic, ob/ob-1α(OH)ase(-/-) mice. Significantly, in contrast to the reduced survival of the ob/ob-klotho(-/-) mice, lowering serum phosphate levels in ob/ob-1α(OH)ase(-/-) mice showed no such compromised survival, despite both mice being hypercholesterolemic.
conclusionThese genetic manipulation studies suggest phosphate toxicity is an important risk factor in obesity that can adversely affect survival.
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