Bioavailability of nanoemulsified conjugated linoleic acid for an antiobesity effect

Abstract

Background:The aim of this study was to enhance the bioavailability of conjugated linoleic acid (CLA), which has low water solubility, using nanoemulsion technology and to evaluate the effects of its improved bioavailability as an antiobesity agent. Methods: The antiobesity effect of nanoemulsified water-soluble conjugated linoleic acid (N-CLA) was evaluated using in vitro and in vivo studies. Differentiated 3T3-L1 adipocytes were treated with CLA and N-CLA to assess their lipolytic effect. Further, to confirm the antiobesity effect of N-CLA, male Sprague-Dawley rats were randomly separated into four groups, ie, a group fed a normal diet, a group fed a high-fat diet (obesity rat model), a CLA-treated group, and an N-CLA-treated group. Results: N-CLA showed a greater lipolytic effect on differentiated 3T3-L1 adipocytes compared with normal CLA. N-CLA enhanced the release of glycerol from triglycerides, which accumulated in differentiated 3T3-L1 adipocytes. Further, N-CLA enhanced leptin secretion to an extent similar to that of orlistat, an antiobesity agent. In an animal obesity model fed a high-fat diet, N-CLA attenuated accumulation of triglycerides, total cholesterol, and low-density lipoprotein cholesterol in serum, and also significantly decreased the volume of triglycerides and cholesterol in liver tissue. Conclusion: These results indicate that N-CLA has a greater antiobesity effect than CLA as a result of its improved bioavailability.

Drugs Involved in Dyslipidemia and Obesity Treatment: Focus on Adipose Tissue

“…Orlistat inhibits gastric and pancreatic lipases [ 158 ], enzymes that play a pivotal role in the digestion of dietary fat. Thus, orlistat by impairing fat intestinal absorption leads to body weight reduction (weight loss of 3% ( https://www.gene.com/download/pdf/xenical_prescribing.pdf , accessed on 15th February 2017)), improves glucose intolerance, and ameliorates lipid parameters (total cholesterol and LDL) [ 159 , 160 ]. Interestingly, orlistat can reverse liver steatosis but not adipocyte hypertrophy [ 159 ].…”

“…Orlistat partially inhibits lipolysis in adipocytes by suppressing AMPK activation and decreasing the AMP/ATP ratio induced by forskolin, isoproterenol, and IBMX (agents able to increase cAMP levels), without altering PKA activity and cAMP levels [ 161 ]. On the other hand, others reported that orlistat has a lipolytic effect, inducing TG degradation in AT and the liver [ 160 ].…”