Sindrom metabolik: Perbedaan antara revisi

Sindrom metabolik dihubungkan dengan risiko munculnya [[penyakit kardiovaskular]] dan [[diabetes melitus tipe 2]]. <ref name="pmid24711954">{{Cite journal|year=2014|title=A comprehensive review on metabolic syndrome|journal=Cardiology Research and Practice|volume=2014|pages=1–21|doi=10.1155/2014/943162|pmc=3966331|pmid=24711954|vauthors=Kaur J}}</ref> <ref name="10.13140/RG.2.1.4502.4804">{{Cite journal|last=Felizola|first=Saulo JA|year=2015|title=Ursolic acid in experimental models and human subjects: Potential as an anti-obesity/overweight treatment?|doi=10.13140/RG.2.1.4502.4804}}{{MEDRS|date=October 2017}}</ref> Di Amerika Serikat, sekitar seperempat dari populasi orang dewasa memiliki sindrom metabolik, dan [[prevalensi]] meningkat dengan bertambahnya usia. <ref name="Falkner-2014">{{Cite journal|date=July 2014|title=Prevalence of metabolic syndrome and obesity-associated hypertension in the racial ethnic minorities of the United States|journal=Current Hypertension Reports|volume=16|issue=7|pages=449|doi=10.1007/s11906-014-0449-5|pmc=4083846|pmid=24819559|vauthors=Falkner B, Cossrow ND}}</ref> <ref name="pmid23810877">{{Cite journal|date=August 2013|title=Prevalence and trends of metabolic syndrome in the adult U.S. population, 1999–2010|journal=Journal of the American College of Cardiology|volume=62|issue=8|pages=697–703|doi=10.1016/j.jacc.2013.05.064|pmc=3756561|pmid=23810877|vauthors=Beltrán-Sánchez H, Harhay MO, Harhay MM, McElligott S}}</ref>

Tanda kunci sindrom metabolik adalah [[Perut buncit|obesitas sentral]], juga dikenal sebagai visceral, adipositas pola pria atau berbentuk apel. Hal ini ditandai dengan akumulasi [[Adipositas|jaringan adiposa]] terutama di sekitar pinggang dan badan. <ref>{{Cite web|url=http://www.diabetes.co.uk/diabetes-and-metabolic-syndrome.html|title=Metabolic Syndrome|date=15 January 2019|website=Diabetes.co.uk}}</ref> Tanda-tanda lain dari sindrom metabolik yaitu tekanan darah tinggi, penurunan kolesterol HDL serum puasa, peningkatan kadar [[trigliserida]] serum puasa, [[ Glukosa puasa terganggu|gangguan glukosa puasa]], resistensi insulin, atau prediabetes. Penyakit terkait yaitu [[ Hiperurisemia|hiperurisemia]]; [[penyakit perlemakan hati non-alkoholik]] (terutama pada orang yang juga [[Kegemukan|obesitas]]) yang berkembang menjadi [[ Penyakit hati berlemak nonalkohol|penyakit perlemakan hati nonalkohol]] ; [[sindrom ovarium polikistik]] pada wanita, dan [[disfungsi ereksi]] pada pria; dan [[ Acanthosis nigricans|acanthosis nigricans]].

Keterlibatan [[ Sistem endocannabinoid|sistem endokannabinoid]] dalam pengembangan sindrom metabolik sangatlah besar.<ref name="ECS - metabolic disorders">{{Cite book|title=Endocannabinoids|last=Gatta-Cherifi|first=Blandine|last2=Cota|first2=Daniela|year=2015|isbn=978-3-319-20824-4|series=Handbook of Experimental Pharmacology|volume=231|pages=367–91|chapter=Endocannabinoids and Metabolic Disorders|doi=10.1007/978-3-319-20825-1_13|pmid=26408168|quote=The endocannabinoid system (ECS) is known to exert regulatory control on essentially every aspect related to the search for, and the intake, metabolism and storage of calories, and consequently it represents a potential pharmacotherapeutic target for obesity, diabetes and eating disorders.&nbsp;... recent research in animals and humans has provided new knowledge on the mechanisms of actions of the ECS in the regulation of eating behavior, energy balance, and metabolism. In this review, we discuss these recent advances and how they may allow targeting the ECS in a more specific and selective manner for the future development of therapies against obesity, metabolic syndrome, and eating disorders.}}</ref> <ref name="ECS - MS">{{Cite journal|author-link3=Alexandros Makriyannis|date=March 2008|title=Pharmacotherapeutic targeting of the endocannabinoid signaling system: drugs for obesity and the metabolic syndrome|journal=Physiology & Behavior|volume=93|issue=4–5|pages=671–86|doi=10.1016/j.physbeh.2007.11.012|pmc=3681125|pmid=18155257|quote=The etiology of many appetitive disorders is characterized by a pathogenic component of reward-supported craving, be it for substances of abuse (including alcohol and nicotine) or food. Such maladies affect large numbers of people as prevalent socioeconomic and healthcare burdens. Yet in most instances drugs for their safe and effective pharmacotherapeutic management are lacking despite the attendant medical needs, collateral adverse physical and psychological effects, and enormous global market potential. The endocannabinoid signaling system plays a critical role in motivational homeostasis as a conduit for reward stimuli and a positive modulator of brain reward circuits. Endocannabinoid-system hyperactivity through CB1 receptor transmission is considered contributory to a range of appetitive disorders and, hence, is a major focus of contemporary pharmaceutical research.|vauthors=Vemuri VK, Janero DR, Makriyannis A}}</ref> <ref name="AA and endocannabinoids">{{Cite journal|date=June 2015|title=Regulation of inflammation by cannabinoids, the endocannabinoids 2-arachidonoyl-glycerol and arachidonoyl-ethanolamide, and their metabolites|journal=Journal of Leukocyte Biology|volume=97|issue=6|pages=1049–70|doi=10.1189/jlb.3RU0115-021R|pmid=25877930|vauthors=Turcotte C, Chouinard F, Lefebvre JS, Flamand N}}</ref> Kelebihan produksi endokannabinoid dapat menyebabkan disfungsi [[ Sistem Penghargaan|sistem penghargaan]]<ref name="ECS - MS" /> dan menyebabkan [[ Disfungsi eksekutif|disfungsi eksekutif]] (misalnya melalaikan keterlambatan yang terganggu), yang pada gilirannya akan melangsungkan perilaku tidak sehat. Otak sangat penting dalam pengembangan sindrom metabolik, memodulasi karbohidrat perifer, dan metabolisme lipid. <ref name="ECS - metabolic disorders" /> <ref name="ECS - MS" />

Sindrom metabolik dapat disebabkan oleh makan berlebih dengan gula atau fruktosa, terutama bersamaan dengan diet tinggi lemak.<ref>{{Cite journal|date=June 2004|title=Role of fatty acid composition in the development of metabolic disorders in sucrose-induced obese rats|journal=Experimental Biology and Medicine|volume=229|issue=6|pages=486–93|doi=10.1177/153537020422900606|pmid=15169967|vauthors=Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H}}</ref> Kelebihan pasokan [[ Asam lemak omega-6|asam lemak omega-6]], terutama [[asam arakidonat]] (AA), merupakan faktor penting dalam [[patogenesis]] sindrom metabolik. Asam arakidonat (dengan prekursornya - [[ Asam linoleat|asam linoleat]] ) berfungsi sebagai substrat untuk produksi mediator inflamasi yang dikenal sebagai [[eikosanoid]], sedangkan senyawa yang mengandung asam arakidonat [[ Diacylglycerol|diasilgliserol]] (DAG) merupakan prekursor untuk endocannabinoid [[ 2-arachidonoylgliserol|2-arachidonoylglycerol]] ( 2-AG) sementara [[ Asam lemak amida hidrolase|asam lemak amida hidrolase]] (FAAH) memediasi metabolisme [[ Anandamide|anandamida]] menjadi [[asam arakidonat]].<ref name="FAAH">{{Cite journal|date=Dec 1994|title=Formation and inactivation of endogenous cannabinoid anandamide in central neurons|url=http://www.escholarship.org/uc/item/0kh020xm|journal=Nature|type=Submitted manuscript|volume=372|issue=6507|pages=686–91|bibcode=1994Natur.372..686D|doi=10.1038/372686a0|pmid=7990962|vauthors=Di Marzo V, Fontana A, Cadas H, et al.}}</ref> <ref name="AA and endocannabinoids">{{Cite journal|date=June 2015|title=Regulation of inflammation by cannabinoids, the endocannabinoids 2-arachidonoyl-glycerol and arachidonoyl-ethanolamide, and their metabolites|journal=Journal of Leukocyte Biology|volume=97|issue=6|pages=1049–70|doi=10.1189/jlb.3RU0115-021R|pmid=25877930|vauthors=Turcotte C, Chouinard F, Lefebvre JS, Flamand N}}</ref> Anandamida juga dapat diproduksi dari [[ N-Acylphosphatidylethanolamine|''N'' -asilfosfatidiletanolamin]] melalui beberapa jalur.<ref name="AA and endocannabinoids" /> Anandamida dan 2-AG juga dapat dihidrolisis menjadi asam arakidonat, berpotensi menyebabkan peningkatan sintesis eikosanoid.<ref name="AA and endocannabinoids" />