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Background: Diabetic nephropathy is a major microvascular complication of diabetes and a primary cause of end-stage renal disease worldwide. This study was designed to assess whether control of hyperglycemia with empagliflozin, a new sodium glucose cotransporter (SGLT) 2 inhibitor could improve the renal functions in streptozotocin induced diabetic rats. Thirty two adult male albino rats were randomly assigned into four equal groups. Group I; non diabetic control, Group II; non diabetic rats treated with empagliflozin, group III; diabetic rats and group IV; diabetic rats treated with empagliflozin. Diabetic rats treated with empagliflozin showed significant increase in body weight and significant reduction in Kidney weight, blood glucose and glycated haemoglobin (HbA1c) levels. Empagliflozin also produced significant decrease in blood urea nitrogen (BUN), serum creatinine, urinary albumin excretion (UAE), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and transforming growth factor beta-1 (TGF-β1). It also attenuated Kidney tissue oxidative stress. Empagliflozin showed a renoprotective effect in streptozotocin induced diabetic rats through its glucose lowering effect and by reducing oxidative stress, inflammation, fibrosis and histopathological alterations. SGLT-2 inhibitor seems to be a promising therapeutic strategy for managing diabetes mellitus to slow the progression of diabetic nephropathy.

Osteoporosis is one of the most prevalent bone diseases especially among postmenopausal women. This study was conducted on 36 female rats divided into three equal groups; i) Sham-operated, ii) Ovariectomized (OVX), iii) Leptin treated ovariectomized group. At the end of experiment, blood was collected for measurement of serum alkaline phosphate (ALP), calcium (Ca), phosphorus (P), osteocalcin, receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG). Urine was collected for measurement of urinary deoxypyridoline/creatinine (DPY/Cr). After eight weeks of treatment, administration of leptin inhibited OVX-induced weight gain with uterotrophic effect, decreased bone turnover markers (urinary DPY/Cr, serum osteocalcin and serum ALP) and serum RANKL while it resulted in significant increase in serum calcium and OPG. Moreover, it markedly decreased expression of RANKL and increased expression of OPG in proximal femur, and thus lowered the RANKL/OPG ratio. These findings suggests that the anti-osteoporotic effect of leptin was by inhibiting osteoclastogenesis via modulating RANKL/OPG ratio. Leptin had potential to be developed as alternative therapeutic agents of osteoporosis induced by postmenopause. Keywords • Leptin • Osteoporosis • Bone markers • RANKL • OPG • Osteoclastogenesis Bull. of Egyp. Soc. Physiol. Sci.

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Background: Ischemic stroke is a major cause of death and disability worldwide. Despite decades of intense research, the beneficial treatment of stroke remains limited. Adiponectin, a circulating adiposederived hormone, has beneficial actions on cardio-and cerebrovascular disorders. A low level of plasma adiponectin is associated with ischemic cerebrovascular disease. In the present study, the role of adiponectin in the pathogenesis of acute cerebral injury was investigated. Rats were divided into three groups: (i) Sham operated group; (ii) Ischemia/reperfusion (I/R) group, rats were subjected to one hour middle cerebral artery occlusion followed by 23 hours of reperfusion (I/R); (iii) Adiponectin-treated group, adiponectin (0.5 mg/kg) was injected through jugular vein 10 minutes after the onset of reperfusion. Adiponectin supplementation improved neurological function and resulted in reduction in infarction size, and brain edema, brain contents of malondialdehyde (MDA), brain levels of nitric oxide (NO) levels, tumor necrosis factor-alpha (TNF-α) and caspase-3. Moreover it enhanced SOD (superoxide dismutase). Results of the present study demonstrate that adiponectin exerts a potent cerebroprotective effect against I/R injury through its anti-inflammatory and anti-oxidant action and anti-apoptotic mechanisms. It might be a potential target for ischemic stroke therapy.