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The Health Promotion Board (HPB) has developed the Clinical Practice Guidelines (CPG) on Obesity to provide health professionals in Singapore with recommendations for evidence-based interventions for obesity. This article summarises the introduction, epidemiology and executive summary of the key recommendations from the HPB-MOH CPG on Obesity for the information of SMJ readers. The chapters and page numbers mentioned in the reproduced extract refer to the full text of the guidelines, which are available from the Health Promotion Board website: http://www.hpb.gov.sg/cpg-obesity. The recommendations should be used with reference to the full text of the guidelines. Following this article are multiple choice questions based on the full text of the guidelines.

Solvation behaviors of N-isopropylacrylamide (NIPAM) in water/methanol mixtures are investigated by molecular dynamics simulations. The results indicate that NIPAM-solvent interactions are weakened with the increase of methanol mole fractions (x(methanol)) from 0.25 to 0.80, rationalizing the reentrant coil-to-globule-to-coil transition behaviors of poly(N-isopropylacrylamide) in the mixed solvents. Interestingly, hydrogen-bonded water/methanol clusters are abundant in binary mixed solvents, leading to the decrement of NIPAM-solvent interactions. To better understand the intermolecular interactions in the water/methanol complex clusters, the structures of pure water and methanol clusters are also studied for a comparison. Although the amount of water clusters decreases with an increase in x(methanol), the structure of water clusters stays stable, and hydrogen-bonded networks are not essentially disrupted. As for methanol molecules, they prefer to form short nonbranched chainlike hydrogen-bonded clusters. However, most of the chainlike hydrogen-bonded methanol clusters are broken in water-rich solutions, leaving the little probability for the formation of dimeric and trimeric methanol clusters.

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Background and Aims Several studies have shown that expression of hepatic fibroblast growth factor 21 (FGF21) can be stimulated by glucagon‐like peptide 1 (GLP‐1)–based diabetes drugs. As GLP‐1 receptor (GLP‐1R) is unlikely to be expressed in hepatocytes, we aimed to compare such stimulation in mice and in mouse hepatocytes, determine the involvement of GLP‐1R, and clarify whether FGF21 mediates certain functions of the GLP‐1R agonist liraglutide. Approach and Results Liver FGF21 expression was assessed in mice receiving a daily liraglutide injection for 3 days or in mouse primary hepatocytes (MPHs) undergoing direct liraglutide treatment. The effects of liraglutide on metabolic improvement and FGF21 expression were then assessed in high‐fat diet (HFD)‐fed mice and compared with the effects of the dipeptidyl‐peptidase 4 inhibitor sitagliptin. Animal studies were also performed in Glp1r−/− mice and liver‐specific FGF21‐knockout (lFgf21‐KO) mice. In wild‐type mouse liver that underwent RNA sequencing and quantitative reverse‐transcription PCR, we observed liraglutide‐stimulated hepatic Fgf21 expression and a lack of Glp1r expression. In MPHs, liraglutide did not stimulate Fgf21. In mice with HFD‐induced obesity, liraglutide or sitagliptin treatment reduced plasma triglyceride levels, whereas their effect on reducing body‐weight gain was different. Importantly, increased hepatic FGF21 expression was observed in liraglutide‐treated mice but was not observed in sitagliptin‐treated mice. In HFD‐fed Glp1r−/− mice, liraglutide showed no beneficial effects and could not stimulate Fgf21 expression. In lFgf21‐KO mice undergoing dietary challenge, the body‐weight‐gain attenuation and lipid homeostatic effects of liraglutide were lost or significantly reduced. Conclusions We suggest that liraglutide‐stimulated hepatic Fgf21 expression may require GLP‐1R to be expressed in extrahepatic organs. Importantly, we revealed that hepatic FGF21 is required for liraglutide to lower body weight and improve hepatic lipid homeostasis. These observations advanced our mechanistic understanding of the function of GLP‐1–based drugs in NAFLD.