ABSTRACT
Objective:To observe the effects of Da Chaihutang on Cyclic adenosine monophosphate （cAMP）-response element binding protein （CREB）/peroxisome proliferator-activated receptor-gamma coactivator-1 alpha （PGC-1<italic>α</italic>） pathway in nutritionally obese rats and the protective mechanism on liver mitochondria. Method:A total of 120 8-week-old male SD rats were randomly divided into a control group （<italic>n</italic>=20） and an experimental group （<italic>n</italic>=100）. The rats in the control group were fed on a normal diet， while those in the experimental group were administered with a high-fat feed. Successfully modeled rats were randomly divided into a model group， a positive drug （metformin） group， and low-， medium- and high-dose Da Chaihutang groups （4.25， 8.5， and 17 g∙kg<sup>-1</sup>， respectively）， with 20 rats in each group. After treatment with Da Chaihutang， the body weight， Lee's index， liver mitochondrial membrane potential and mitochondrial ultrastructure， PGC-1<italic>α </italic>expression and CREB phosphorylation of each group were measured and compared. Result:Compared with the control group， the model group showed increased body weight and Lee's index （<italic>P</italic><0.01）， whereas decreased mitochondrial membrane potential， PGC-1<italic>α</italic> expression， and CREB phosphorylation level （<italic>P</italic><0.01）. As compared with the model group， Da Chaihutang significantly reduced the body weight and Lee's index of obese rats （<italic>P</italic><0.05， <italic>P</italic><0.01）， enhanced liver mitochondrial membrane potential （<italic>P</italic><0.05， <italic>P</italic><0.01） to protect the integrity of mitochondrial structure， up-regulated PGC-1<italic>α</italic> expression and promoted CREB phosphorylation （<italic>P</italic><0.05， <italic>P</italic><0.01）. Conclusion:Da Chaihutang protects the structure and function of mitochondria and inhibits weight gain in obese rats by activating the CREB/PGC-1<italic>α</italic> pathway.
ABSTRACT
Obesity is one of the leading causes of preventable mortalities in many parts of the globe. The rise in geriatric population due to better treatment opportunities has also emerged as a major public health challenge. Both of these health challenges have impacted developed as well as developing countries. Obesity is attributed as a powerful risk factor of a variety of health problems such as cardiovascular diseases, hypertension, type 2 diabetes, dementia, neuropsychiatric diseases and many more. On the other hand, ageing is a natural process involving a gradual decline in physiological functions and is associated with similar co-morbidities as obesity. This review discusses about the commonalities (termed as ‘Obesageing') between the pathological phenomenon of obesity and normal physiological process of ageing. A unique rodent model of obesageing has been developed (WNIN/Ob) that has characteristics of morbid obesity as well as premature ageing. Such a novel animal model would facilitate the understanding of the complex interplay of different mechanisms that are common to obesity and ageing and help to devise strategies in future to tackle the growing burden of obesity and ageing.
ABSTRACT
Vitamin D has been found to produce therapeutic effects on obesity-associated insulin resistance and dyslipidemia through its potent anti-inflammatory activity, but the precise immunomodulatory mechanism remains poorly understood. In the present study we found that 1,25-dihydroxyvitamin D [1,25(OH)D], the biologically active form of vitamin D, significantly attenuated monosodium glutamate (MSG)-induced obesity and insulin resistance as indicated by body weight reduction, oral glucose tolerance improvement, and a glucose infusion rate increase as detected with hyperinsulinemic-euglycemic clamp. Moreover, 1,25(OH)D not only restored pancreatic islet functions but also improved lipid metabolism in insulin-targeted tissues. The protective effects of 1,25(OH)D on glycolipid metabolism were attributed to its ability to inhibit an obesity-activated inflammatory response in insulin secretory and targeted tissues, as indicated by reduced infiltration of macrophages in pancreas islets and adipose tissue while enhancing the expression of in liver tissue, which was accompanied by increased infiltration of Treg cells in immune organs such as spleen and lymph node as well as in insulin-targeted tissues such as liver, adipose, and muscle. Together, our findings suggest that 1,25(OH)D serves as a beneficial immunomodulator for the prevention and treatment of obesity or metabolic syndrome through its anti-inflammatory effects.
ABSTRACT
Objective To observe the adipose-derived cytokine changes and aggravate cognitive impairment in olanzapine-induced obese rats caused by glucose metabolic disorder.Methods 20 rats fed with ordinary fodder were used as normal control group,olanzapine group of 20 rats fed with olanzapine(1.2 mg · kg-1) and ordinary fodder for 4 weeks.Successfully established experimental model rats induced by olanzapine after 4 weeks.Serum tumor necrosis factor α(TNF-α),interleukins 6 (IL-6) and C-reactive protein (CRP) contents were measured by Elisa.Serum glucose contents were determined by biochemical colorimetric method and blood lipid contents determined with automatic biochemical analyzer.Learning,memory capacity and escape latency were detected with Maze test.Results After administration 4 weeks,the levels of body weight,blood glucose and blood lipid in olanzapine group were higher than those in control group.The serum TNF-α((1.57±0.04) ng/ml),IL-6((127.47±11.38) pg/ml) and CRP ((2.68±0.06) mg/ml) in olanzapine group rised,compared with control group ((0.59±0.03) ng/ml,(96.58± 8.77) pg/ml and (1.86±0.04) mg/ml respectively),the differences were statistically significant(P＜0.05).Electric shocks and escape latency in olanzapine group were higher than those in control group (P＜0.05).The FBS had positive correlation with hs-CRP,IL-6 and TNF-α respectively (r=0.385,0.260,1.280; all P＜0.05).Conclusion Olanzapine can induce metabolic disturbance of blood glucose,blood hpid,and the increase of serum TNF-α,IL-6 and CRP levels in rats.Positive correlation is showed between TNF-of and FBS.Hyperglycemia can promote cell toxicity and leads to cognitive dysfunction in rats.