Mohamed Ahmed, Kailash Prasad, Ahmed Shoker

Consequences of Hypervitaminosis D in NZW Rabbit Model

Introduction

Consequences of hypervitaminosis d in nzw rabbit model. Investigates hypervitaminosis D's impact on kidney function and serum lipids in NZW rabbits, revealing its role in renal insufficiency (calcium-dependent) and aggravated hypercholesterolemia.

Abstract

Background and Aim: This study examines the effect of hypervitaminosis D on serum lipids and on kidney functions in New Zealand White (NZW) rabbit. It aims to study whether renal insufficiency or failure, due to hypervitaminosis D, is calcium-related or not. As well, it also discusses a possible link between hypervitaminosis D and hypercholesterolemia. Methods: Four Groups of six animals each, were divided into: Group I, received regular diet, Group II received regular diet +10,000/day vitamin D2; Group III, received 0.25% cholesterol diet; as well as Groups IV received 0.25% cholesterol diet plus 10,000 IU. Blood samples were taken at the end of the study and examined for Total Cholesterol (TC), Triglycerides (TG), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL), Blood Urea Nitrogen (BUN), Creatinine, Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP), Calcium and Phosphate. As well, 25- hydroxyvitamin D (25 (OH) D) was measured using tandem LC-MS/MS. Results: The initial (0 time) serum TC, TG, LDL, HDL, Creatinine, Calcium, Phosphate and 25 (OH) D levels were not significantly different among different groups including control. At 1- and 2-month time, values from serum TC, TG, LDL, HDL and TC/HDL-C ration of Groups III and IV were significantly different from controls (p<0.05). As well, values from serum 25 (OH) D of Group II and IV were significantly different from controls (p<0.05) at 1- and 2-month time. However, values from serum Creatinine and Calcium of Group II were significantly different from controls (p<0.05) at 1- and 2-month time. Conclusion: Hypervitaminosis D may aggravate hypercholesterolemia, and it also induces renal insufficiency and/ or failure through a calcium-dependent mechanism. -- Highlights: 1. Excessive vitamin D supplementation, particularly when combined with a hypercholesterolemic diet, aggravated hyperlipidemia and elevated serum calcium levels in NZW rabbits. 2. Hypervitaminosis D was associated with increased serum creatinine and hypercalcemia, suggesting potential renal impairment secondary to excessive vitamin D intake

Review

This study investigates the critical health implications of hypervitaminosis D on lipid metabolism and kidney function in a New Zealand White (NZW) rabbit model, offering valuable insights into a potentially under-recognized clinical concern. The research competently establishes that excessive vitamin D intake can lead to hypercalcemia and subsequent renal insufficiency, which is a significant finding well-supported by the reported data for Group II. The experimental design, employing distinct groups to isolate the effects of vitamin D, a high-cholesterol diet, and their combination, is a strength. Furthermore, the inclusion of a comprehensive panel of biochemical markers, coupled with initial baseline measurements, strengthens the reliability of the observed changes over the study period. While the study presents important findings, several aspects require further clarification to enhance its scientific rigor. Firstly, there is an inconsistency in the methodology description regarding blood sampling – stating "at the end of the study" while results mention "1- and 2-month time." A precise timeline for sample collection and whether all parameters were measured at both time points needs to be clearly articulated. More critically, the conclusion that hypervitaminosis D "may aggravate hypercholesterolemia" requires stronger statistical evidence. The abstract indicates that both cholesterol-fed groups (III and IV) were significantly different from controls in lipid profiles, but it does not explicitly state whether Group IV demonstrated a statistically significant *aggravation* compared to Group III. This distinction is crucial for substantiating the claim of aggravation. Additionally, while ALT, AST, and ALP were mentioned in methods, results for these liver enzymes were absent, which might indicate either no significant changes or incomplete reporting. Despite these points for refinement, the study makes a meaningful contribution to understanding the adverse effects of hypervitaminosis D. The robust evidence for hypercalcemia-induced renal impairment highlights a vital area for clinical consideration regarding vitamin D supplementation guidelines. Future iterations of this work would benefit from explicitly comparing the relevant experimental groups (e.g., Group IV vs. Group III for lipid parameters, Group II vs. Group IV for renal/calcium effects) with appropriate statistical analyses to firmly support the conclusions on synergistic effects. Incorporating histopathological examination of renal tissue would also provide definitive evidence of kidney damage. Overall, this research lays important groundwork, prompting further investigation into the intricate interplay between vitamin D status, lipid metabolism, and renal health, with significant implications for public health advice on vitamin D supplementation.

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