Hout choline added 28.9 kcal/g L-glutamic acid, 15.8 kcal/g Laspartic acid, 12.7 kcal/g L-arginine, and ten.five kcal/g L-leucine but choline deficient CDAA 0.two ml/g CCl4 injection NA NA NA NA NAObesityYes No Yes Yes Yes YesInsulin resistanceYes Yes Yes Yes Yes YesSteatosisYes Yes Yes Yes Yes YesNASHYes (mild) Yes Yes (mild) Yes Yes YesFibrosisYes (mild) Yes Yes (mild) Yes Yes YesHCCNo No No No No YesHigh-fat, high sucrose eating plan Long-term low fat- higher carbohydrate diet High-fat eating plan streptozotocin High-fat eating plan Diethylnitrosamine (DEN) High-fat eating plan carbon tetrachloride (CCl4) High-fat, high-fructose and highcholesterol CCl4 Methionine- and choline- deficient diet plan (MCD) Methionine- and choline- deficient eating plan DEN Choline-deficient high-fat diet program Choline-deficient amino acid diet program (CDAA)Yes No Yes Yes Yes YesYes Yes Yes Yes YesYes Yes Yes Yes Yes YesYes Yes Yes Yes Yes YesYes (mild) Yes Yes Yes Yes YesNo Yes Yes Yes Yes YesNo No Yes NoYes Yes Yes YesYes Yes Yes YesYes Yes Yes YesYes Yes Yes YesNo Yes Yes YesCholine-deficient L-amino acid-defined diet CCl4 ob/ob mice db/db mice foz/foz mice db/db mice 25 ml/g DEN Jet lag (12 h:12 h dark/light cycle disrupting just about every 5 days over three weeks by extending the dark cycle 12 h)No Yes Yes Yes Yes YesYes Yes Yes Yes Yes YesYes Yes Yes Yes Yes YesYes No No Yes Yes YesYes No No Yes YesYes No No No Yes YesMOLECULAR METABOLISM 50 (2021) 101190 2021 The CK1 medchemexpress Authors. Published by Elsevier GmbH. This is an open access post under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). www.molecularmetabolism.comTable two e Genetically modified animal models applied to recognize the role of JNK and p38 in NAFLD development. MAPKJNK1 JNK1 JNK1 JNK1 JNK1 JNK1 JNK2 JNK2 JNK1/2 JNK1/2 p38aMouse modelSystemic JNK1 PLK1 manufacturer knockout Adenoviral dominant-negative JNK1 delivery for the liver Systemic antisense oligonucleotides against JNK1 Liver-specific JNK1 knockdown with adenovirus Liver-specific JNK1 knockout Adipose-specific JNK1 knockout Systemic JNK2 knockout Systemic antisense oligonucleotides against JNK1 Systemic Jnk1 nk2Liver-specific JNK1/2 knockout Liver-specific p38a knockoutPhenotypeUnder HFD: decreased body weight, improved hepatic insulin signalling, and decreased steatosis. Under HFD: decreased physique weight, improved insulin sensitivity, and decreased gluconeogenesis. Under HFD: improved insulin sensitivity and hepatic steatosis. No information on physique weight. Under HFD: improved insulin sensitivity, glycolysis, triglyceride secretion, and b-oxidation. Below CD: glucose intolerance, insulin resistance, and hepatic steatosis related with elevated gluconeogenesis and lipogenesis Below HFD: improved physique weight and decreased insulin resistance and hepatic steatosis. Under HFD: no increase in insulin sensitivity and no reduction in adipose tissue mass, but high JNK activation. Below HFD: enhanced insulin sensitivity but increased liver injury, devoid of decreasing steatosis. Below HFD: reduced body weight and enhanced insulin sensitivity Beneath HFD: decreased FA oxidation and ketogenesis, enhancing insulin sensitivity and steatosis by activation of PPARa and FGF21 signalling. Below CD: reduced fasting glucose and impaired gluconeogenesis in an AMPK-dependent manner. Under HFD: increased body weight, fat weight and liver weight. More glucose intolerant. Enhanced steatohepatitis characterised by steatosis and inflammation. Under HFHC: much less steatosis-steatohepatitis and insulin resistance by M2 anti-inflammatory.
