The Impact Of Caffeine On Fat Metabolism Of The Caenorhabditis Elegans

Caffeine is the world’s most widely used food contained in the factor, themain component of tea, coffee, fruit, and it is a methylxanthine alkaloids.In the body, coffee is the main role of the adenosine receptor antagonist,which blocks adenosine receptor binding to lead to the obvious effects ofinsomnia. Because the adenosine receptor and G protein-coupled, whichregulates the cells G protein-coupled signaling pathways including the controlof Ca2+out of energy metabolism, hormone secretion, not only may caffeinebe the role of the central nervous system stimulant, but also play a role onthe body metabolism, hormone levels, which is commonly used as clinicaltreatment of neurasthenia and coma recovery. At present, the role of caffeineon the nervous system, digestive system, cardiovascular system and secretionsystem has been a lot of research, but few studies on energy metabolism,especially in fat metabolism. Now a lot of coffee drinks company and the massmedia declare that caffeine can reduce fat accumulation and increase fatmetabolism with certainty, although there have been some reported in theliterature that caffeine can reduce body fat in mice, but no more clearscientific result can insure the truth for that. So, the comments may haveto produce a series of misleading for people. The questions, such as wethercaffeine can lose weight or not, in another way, how the impact of caffeineon fat metabolism, need more scientific experiments to validate and explore.The purpose of this article is to study the impact of caffeine on the C. elegansfat metabolism, and we hope that the mechanism of the body’s mechanism of actionof caffeine in C. elegans can provide accurate experimental data andtheoretical basis for future in-depth study, at the same time, we also wantto find fat regulatory and related proteins and genes of C. elegans that is not yet clear.In the initial formulation of caffeine on fat metabolism as the maindirection, we had been looking for a simple experimental animals with clearmetabolism, and finalized the Caenorhabditis elegans as the experimental model.Caenorhabditis elegans has a short life cycle and small size, and its genomeoperation is clear and simple. It is tiny and transparent to facilitateobservation, with other unique advantages, it has been widely used in genetics,neurology, pathology and biomedical disciplines. In fat metabolism, the studyfound three fat pathway of C.elegans, the serotonin pathway, the insulinpathway and the life of the DAF-2/transforming growth factor TGF-beta pathway,and their activation can enhance the accumulation of fat. Among them, the SER-6,NHR80, NHR49, the FAT-5, FAT-6and FAT-7are more important regulatoryproteins.In the total fat and total triglyceride detection experiments, we found thatcaffeine significantly increased the accumulation of wild-type C. eleganstotal body fat; RT-PCR experiments confirmed that in the genes of all nematodeto promote fat accumulation, caffeine significantly increased fat-5mRNAlevels, and the rest was no obvious change; gas chromatography results showedthat caffeine changed the composition of the nematode fatty acid ratio, andincreased the ratio of16carbon single unsaturated fatty acids to unsaturatedfatty acids hexadecenoic. These results were similary with that of Pu’er teapowder. In mammals, the fat-5homologous gene SCD1, we had experiment furtherextended to mice and found that Pu’er significantly increased in mice SCD1expression level, and gas chromatography showed that Pu’er tea raised18-carbon unsaturated fatty acid ratio of mice. SCD1played an inportant rolein lipid biosynthesis and carbohydrate metabolism in mice, and SCD1deficiencywoud lead to the reduction of metabolic rate and reduction in insulinconcentration.Type II diabetes drugs such as PPARγ agonists could increaseSCD1expression and activity. Some studies had reported that caffeine couldreduce the plasma glucose concentration in diabetic mice and increased insulin sensitivity, while monounsaturated fatty acids palmitoleic acid as derivedlipid hormone could activate the activity of insulin in muscle and inhibitionof hepatitis, so we did the same analysis on the typical drug rosiglitazone.Then we found that rosiglitazone increased the mouse SCD1and C. elegans fat-5expression, but also raised mice eighteen carbon monounsaturated fatty acidsand nematodes16carbon mono-unsaturated fatty acid ratio. This suggested thatthe hypoglycemic mechanism of tea may be associated with rosiglitazone, andfurther speculated that caffeine may also have the same hypoglycemic effectof Pu’er tea and rosiglitazone. Using a variety of mutant nematode TJ1052,DR1568, BX165, BX107, MT9668, LX636, LX702, CB1376, RB1716, CE541on the sameecoxperimets in order to identify the relative genes in the effect of caffeineincreased fat accumulation and monounsaturated fatty acid proportion, we foundthat the mechanism of caffeine on fat metabolism may be relative with thenuclear regulatory factor mdt-15related.For research on fat metabolism of caffeine, we need more advanced animalto continue explore, this article will not be discussed.