Abstract

Hypovitaminosis D is a severe global public health issue. Vitamin D is a fat-soluble secosteroid hormone that may be obtained by diet as well as sun exposure. The efficacy of the vitamin D receptor and vitamin D activating enzyme present in tissues and cells, along with the influence of vitamin D on the musculoskeletal system, support vitamin D's extensive functions. Insufficient vitamin D intake, results in hepatic, renal, skin, and hematological problems which signify vitamin D deficiency. A heat-dependent phase in the synthesis of vitamin D transforms 7-dehydrocholesterol into previtamin D 3 , which is subsequently isomerized into cholecalciferol. The present investigation demonstrates the effect of a long-term inadequate diet on body weight, food intake, and hematological parameters. In this study, female Swiss albino mice were divided into three groups: the control group received standard feed, the vitamin-D-supplemented group received cholecalciferol (1000IU/kg), and the vitamin-D deficient group was fed with a diet lacking in vitamin D for 90 days. Vitamin-D deficient animal group had higher levels of parathyroid hormone and lower levels of 25 hydroxy vitamin D [25(OH)D] in their serum as compared to control animals (p < 0.0001). A substantial decrease in hemoglobin, red blood cells, white blood cells and hematocrit values was observed in the vitamin-D deficient group, along with a significant increase in platelet number. Our findings conclude that consuming a long-term vitamin D-deficient diet changes hematological, dietary, and body weight factors and may result in severe in long-term health problems. • Hypovitaminosis D is inversely proportional with PTH serum level in long term consumption of vitamin D deficient diet. • Daily food consumption of a vitamin D deficient diet resulted in noticeably changed hematological indicators and minor alterations in weight factors. • Vitamin D supplementation in regular basis improve in 25(OH)D serum level and moderately balance PTH. • Higher PTH level and hypocalcemia is directly associated with renal hydroxylation in vitamin D metabolism.

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