# Alkaline Water Mitigates Bone Loss in Streptozotocin-Induced Type II Diabetic Rats

## TL;DR

This study shows that drinking alkaline Zamzam water helps reduce bone loss in diabetic rats by improving bone formation and reducing bone breakdown.

## Contribution

The study demonstrates the novel protective effect of Zamzam water on diabetes-induced osteoporosis in rats.

## Key findings

- ZW increased bone formation markers like osteocalcin and alkaline phosphatase in diabetic rats.
- ZW decreased bone resorption markers such as NTX-1, DPD, and TRAP-5b in diabetic rats.
- X-rays showed improved vertebral bone structure in diabetic rats consuming ZW.

## Abstract

Background

A decline in bone mineral density is a defining feature of osteoporosis, which is a prevalent bone complication associated with diabetes. This study aims to shed light on the protective effect of Zamzam water (ZW), a famous alkaline water, on diabetes-induced osteoporosis.

Methodology

Of a total of 40 male rats, 10 male rats each were divided into the following four groups: group I (normal control rats), group II (ZW group), group III (diabetic rats), and group IV (DM + ZW). Anteroposterior and lateral X-rays were taken of the rats in each group before the end of the experiment. The study assessed serum levels of inflammatory markers including interleukin 6, interleukin-1 beta, and tumor necrosis factor-alpha; bone formation markers including osteocalcin (OC); alkaline phosphatase (ALP); and bone resorption markers including the N-terminal telopeptide of collagen type I (NTX-1), bone deoxypyridinoline (DPD), and tartrate-resistant acid phosphatase 5b (TRAP-5b).

Results

Rats with diabetes who consumed ZW exhibited a significant (p < 0.001) increase in OC and ALP bone formation markers and a decrease in NTX-1, DPD, and TRAP-5b bone resorption markers, with improvements in the X-ray image of the vertebral column at the L6 vertebra level.

Conclusions

ZW improved diabetes-induced osteoporosis in rats by enhancing osteoblastic activity and downregulating osteoclastic activity.