الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Insulin resistance acts as a key link between obesity and T2DM and understanding how obesity causes insulin resistance will improve knowledge of T2DM and ability to treat obesity-related complications.
High Fat Diet (HFD) has also been utilized to model chronic inflammation, which is an important pathogenic mechanism of T2DM. The HFD mediated chronic inflammation is marked by increased TNF-α, IL-1β, and IL-6 in the circulation.
JNKs are serine threonine protein kinases that phosphorylate Jun family members. Components of activator protein 1 (AP-1) transcription factors are triggered by pro inflammatory cytokines such as TNF-α and IL-1β as well as environmental and geno toxic stressors.
JNK was proposed to drive insulin resistance in obesity by distinct mechanisms including direct inhibition phosphorylation of insulin receptor substrates 1and 2, promotion of metabolic inflammation, promotion of metabolic efficiency and adiposity.
Obesity in NAFLD is associated with dysfunctional adipose tissue and lipotoxicity which promotes insulin resistance and pancreatic β-cell dysfunction.
SOD one of increased oxidative stress plays a major role in the etiology of diabetes and its complications.
The vitamin D receptors are widely distributed in more than 38 tissues. Macrophages and dendrite cells constitutively express vitamin D receptors, which indicate that vitamin D plays an important role in regulating the inflammatory response. Vitamin D insufficiency is a potential contributor to insulin resistance and obesity.
The present study aimed to investigate the protective effect of vitamin D (as anti- inflammatory) by suppressing the expression of inflammatory cytokine C-Jun N-terminal kinase (JNK) in rat models of diabetic liver complications.
The present study was carried on 30 male albino rats, with body weight 100–150 grams. The period of the experiment was 16 weeks.
Rats were randomly divided into two groups:
group (I): (control)
Included ten rats that were fed a regular standard chow diet(60% carbohydrates,5% fat and 18% protein). (109) (109)
group (II):
Included twenty rats that were fed a high fat diet HFD (22% fat, 48% carbohydrate, 20% protein) for 8 weeks.
After 8 weeks from start of the diet regimen, all rats of group II received a single low dose of STZ (30 mg/kg). Rats of the control group (group I) received a single IP injection of ml of sodium citrate buffer only.
One week later, random blood glucose level of all rats were measured. Diabetes was confirmed by the detection of hyperglycemia. Half of the T2DM model rats (n=10) were randomly allocated to the vitamin D-treatment.
group IIA (vitamin D treated group):
Ten diabetic rats received vitamin D orally with a dose of (0.03 µg/kg/day) dissolved in corn oil for 8 weeks.