Vitamins For Weight Loss And Metabolism

In cell culture studies, curcumin treatment suppressed palmitatemediated insulin resistance, inhibited the ubiquitinproteasome system, reduced the endoplasmic reticulum protein aggregation and activated the autophagy signaling in human umbilical vein endothelial cells. The suggested antidiabetic mechanisms of curcumin effects are ameliorating bcell dysfunction, insulin signaling, glucagon like peptide secretion, and reducing glucose intolerance, hyperglycemia, hyperinsulinemia, HOMAIR level, hyperlipidemia, islet apoptosis and necrosis etc. Therefore, these finding demonstrate that curcumin supplementation in diabetic population may be beneficial.In addition, curcumin inhibited the phosphorylation of MAPK, JNK, p and ERK thereby rescue the differentiation of TL cells into adipocytes. In addition, curcumin treatment reduces the incidence of obesity and its associated risk factors, mainly due to its antioxidant and antiinflammatory activities. It was concluded that curcumin and vitamin E supplementation modulate hepatic antioxidant gene expression during hypothyroidism. Curcumin administration significantly reduced the level of LPO in cerebellum and cerebral cortex of propylthiouracilinduced hypothyroidism in rats.In addition, curcumin reversed the decreased level of translated products SOD and SOD in rats with hypothyroidism. Interestingly, an earlier study suggested that, vitamin E and curcumin administration restore the activity of serum transaminase, altered rectal temperature and hepatic histoarchitecture in rats with hypothyroidism induced by npropylthiouracil. Interestingly, curcumin reduced the activity of SOD, SOD and SOD in cerebral cortex, while enhanced the SOD and SOD activity in the cerebellum of reasch Fipronil hyperthyroid rat. In another study, curcumin and vitamin E administration reversed the reduced levels of hepatic SOD and CAT.Besides, curcumin administration upregulated the expression of glutathione peroxidase and glutathione reductase in rat liver.In the same study, cotreatment of curcumin along with vitamin E alleviated oxidative stress and liver damage in lthyroxine induced hyperthyroid rats. Further, lthyroxine induced hyperthyroidism and its associated increase in activity of ALT and AST in rat serum were reduced by curcumin and vitamin E treatment resulting in hepatoprotection. These finding suggest that, curcumin administration exerts neuromodulatory and hepatoprotective activity during hyperthyroidism mainly due to its antioxidant effect.In animal model, curcumin administration ameliorated microarchitecture of tibia bone through downregulation of MMP expression, inhibition of osteoprotegerin RANK ligandRANK signaling and the activation of microRNA in dexamethasone treated mice. Mechanistically curcumin treatment ameliorated bone deteriorations through the activation of miR via suppressing MMP. Recently, report suggests that curcumin reversed hindlimb suspensioninduced bone loss in rats via upregulation of vitamin D receptor expression and attenuation of oxidative stress. These evidences of curcumin administration supporting its potential for management of osteoporosis. Curcumin reduce the risk of osteoporosis via several mechanisms including reduction of apoptosis, amelioration of mitochondrial membrane function, PKB phosphorylation, microRNA activation, osteoblasts proliferation etc.It is characterized by diarrhea, abdominal pain, bleeding, anemia, and weight loss.Crohns disease can affect the whole gastrointestinal tract, while ulcerative colitis usually involves colonic mucosa. In a randomized, doubleblind trial, administration of NCB enema once daily for weeks showed better improvement in disease activity when observed through endoscopy study in patients with mildtomoderate distal ulcerative colitis. Further, in a multicentred, doubleblind, placebocontrolled trial, curcumin treatment appeared to be a safe and promising drug candidate for maintaining remission in ulcerative colitis patients.

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