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Obesity is a chronic metabolic disease that involves excessive accumulation of fat in white adipose tissue (WAT). Apart from storing excess fats, WAT also serves as an important endocrine organ secreting adipocytokines such as adiponectin and leptin. Adiponectin and leptin bind to their transmembrane receptors adiponectin receptor 1 (AdipoR1)/adiponectin receptor 2 (AdipoR2) and Ob-R , respectively, and mediate their effect on metabolism by regulating multiple downstream targets. Dietary fat is considered the main culprit behind obesity development. Numerous preclinical studies have highlighted role of essential polyunsaturated fatty acids (PUFAs), particularly n-3 PUFAs, in prevention of obesity. Despite emerging data, there still is no clear understanding of the mechanism of action of n-3 PUFAs and n-6 PUFAs on adipose tissue function in two functionally and anatomically different depots of WAT: visceral and subcutaneous. We designed this study using a high fat diet (HFD) fed rodent model of obesity to test our hypothesis that n-3 and n-6 PUFAs possibly differentially modulate adipokine secretion and downstream metabolic pathways such as peroxisome proliferator-activated receptor-γ (PPAR-γ), protein kinase B (AKT)-forkhead box O1 (FOXO1), and Janus kinase-signal transducer and activator of transcription in obesity. The results of the current study showed that n-3 PUFAs upregulate the expression of AdipoR1/R2 and ameliorate the effects of HFD by modulating adipogenesis via PPAR-γ and by improving glucose tolerance and lipid metabolism via AKT-FOXO1 axis in fish oil fed rats. However, n-6 PUFAs did not show any remarkable change compared with HFD fed animals. Our study highlights that n-3 PUFAs modulate expression of various targets in adiponectin and leptin signaling cascade, bringing about an overall reduction in obesity and improvement in adipose tissue function in HFD induced obesity. Graphical representation of effect of n-3 and n-6 PUFAs on white adipose tissue function in high-fat-diet–induced rodent model of obesity. n-3 PUFA supplementation led to an increased expression of adiponectin receptors AdipoR1/R2, resulting in activation of downstream targets PPAR-γ and AKT with specific inhibition of FOXO-1 in subcutaneous WAT, resulting in a beneficial effect on high-fat-diet–induced obesity by increasing adipogenesis, energy expenditure, lipid oxidation, glucose metabolism, and suppression of inflammation. n-6 PUFA supplementation did not show any improvement in adiponectin/leptin mediated signaling. The green arrows signify increased levels and red arrows signify decreased levels. Dotted arrows signify no effect on the downstream target. ACC, acetyl-CoA carboxylase; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; AKT, protein kinase B; AMPK, AMP-activated protein kinase; FOXO1, forkhead box O1; HFD, high-fat diet; JAK-2, Janus kinase 2; Ob-R, leptin receptor; PGC1α, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha; PI3K, phosphoinositide 3-kinase; PPAR, peroxisome proliferator-activated receptor; PUFA, polyunsaturated fatty acid; STAT3, signal transducer and activator of transcription 3; SWAT, subcutaneous white adipose tissue; UCP1, uncoupling protein 1; WAT, white adipose tissue. [Display omitted] [ABSTRACT FROM AUTHOR]

Method: In high fat diet induced obese rats, obesity-related characteristics, including body weight, serum biochemical parameters were assessed. At the end of the experimental histological analysis were carried out. Obesity was induced in Wistar rats using a HFD for first 25days. Then from 25th day to 50th day of study F. racemosa is given in dose of 90 mg/kg and 270mg/kg along with HFD. On 0, 25th, 50th day, body weight, histological changes and other parameters were recorded. Result: Bark powder of F. racemosa significantly reduced the absolute body weight. Ingestion of HFD containing F. racemosa to rat exhibited reduction in lipid parameters. High dose (270 mg/kg b. w) of F. racemosa significantly reduced the levels of triglyceride and VLDL whereas there were few differences observed in LDL and cholesterol. Treatment groups do not exhibited any substantial decrease in BSL. Minimal changes (+1) are found in liver tissues of F. racemose and B. prionitis treated groups. Furthermore, there is a mild fatty deposition is found. Conclusion: The results imply that F. racemose (at higher dose 270 mg/kg body) has anti-obesity effects in obesity-induced rats. [ABSTRACT FROM AUTHOR]

The study investigated how an extract of Sporidiobolus pararoseus (S.p.) affects lipid metabolism in Kunming mice that were obese as a result of being fed a high-fat diet; the control group were administered Max EPA fish oil. Ten mice were randomly selected from a pool of 60 mice for the control group and the remaining 50 mice were fed with a high-fat diet to establish a dyslipidemia model. After 4 weeks, these 50 mice were randomly distributed among 5 groups: high-fat model group; Max EPA group; and 3 groups of mice fed different doses of S.p. extract (low dose, medium dose, and high dose). After 8 weeks, the mice were sacrificed and the relevant parameters were measured. Compared with the high-fat model group, the group administered the high dose of S.p. extract showed significantly decreased body mass and serum levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol, and increased levels of high-density lipoprotein cholesterol. The results from RT-PCR showed that the mRNA expression of sterol regulatory element-binding protein 1c, fatty acid synthesis enzyme, and acetyl-CoA carboxylase was lower in the groups supplemented with S.p. extract than in the high-fat model group, whereas the expression of carnitine palmitoyltransferase 1 was higher in the group supplemented with S.p. extract than in the high-fat model group. Our results suggest that taking S.p. extract could benefit patients with dyslipidemia. Therefore, S.p. extract should be developed as a dietary supplement to improve lipid metabolism in obese people.