Research library

Key finding

During 28 days in diet-induced obese mice, 5A1MQ limited weight and fat gain, improved glucose and insulin measures, and reduced several markers of fatty-liver pathology.

Key finding

A selective NNMT inhibitor reduced body weight, white-fat mass, adipocyte size, and total cholesterol in diet-induced obese mice; cell experiments also found lower lipogenesis and higher intracellular NAD+ and SAM.

Key finding

Combining NNMT inhibition with a lower-calorie diet accelerated fat and weight loss in obese mice and brought body composition and liver-fat measures close to those of lean controls.

Key finding

After muscle injury in aged mice, NNMT inhibition increased muscle-stem-cell activity, produced larger regenerated fibres, and raised peak muscle torque by about 70% versus controls.

Key finding

A validated rat assay measured substantial exposure after oral and intravenous 5-AMQ, including mean oral bioavailability of 38.4% and an oral terminal half-life of about 6.9 hours.

Key finding

There were minimal microbiome differences between lean and obese controls, suggesting that diet composition and adiposity had limited effects.

Key finding

Nicotinamide N-methyltransferase (NNMT) is a metabolic regulator that catalyzes the methylation of nicotinamide (Nam) using the co-factor S-adenosyl-L-methionine to form 1-methyl-nicotinamide (MNA).

Key finding

In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes.

Key finding

Nicotinamide-N-methyltransferase (NNMT) is a cytosolic enzyme catalyzing the transfer of a methyl group from S-adenosyl-methionine (SAM) to nicotinamide (Nam).

Key finding

Patients with manifest type 2 diabetes have a significantly (approximately twofold) higher NNMT expression both in omental and subcutaneous WAT compared with controls.

Key finding

The enzyme nicotidamide-N-methyltransferase (NNMT) regulates adipose tissue energy expenditure through increasing nicotinamide adenosine dinucleotide (NAD+) content.

Key finding

Obesity is a major health problem, and although caloric restriction and exercise are successful strategies to lose adipose tissue in obese individuals, a simultaneous decrease in skeletal muscle mass, negatively effects metabolism and muscle function.

Key finding

Nicotinamide N-methyltransferase (NNMT) is a fundamental cytosolic biotransforming enzyme that catalyzes the N-methylation of endogenous and exogenous xenobiotics.

Key finding

Obesity is associated with adipose tissue dysfunction through the differentiation and expansion of pre-adipocytes to adipocytes (hyperplasia) and/or increases in size of pre-existing adipocytes (hypertrophy).

Key finding

Nicotinamide N-methyltransferase (NNMT) is a methylase, and its expression is positively correlated with obesity and insulin resistance.

Key finding

Nicotinamide N-methyltransferase (NNMT) is a novel regulator, shown recently to regulate adipose tissue energy expenditure partly through changing NAD + content, which is essential for mitochondrial.

Key finding

Glucose availability regulates NNMT expression via an mTOR-dependent mechanism.

Key finding

As obesity develops, body weight predicts NNMT activity in white adipose tissue, but not in any other tissue, consistent with a specific role of adipose-tissue NNMT in the regulation of body weight.

Key finding

Non-alcoholic fatty liver disease (NAFLD), characterized by abnormal lipid accumulation in hepatocytes, is a prevalent metabolic disorder strongly linked to insulin resistance and obesity.

Key finding

Metabolic syndrome (MetS) represents a constellation of metabolic abnormalities, typified by obesity, hypertension, hyperglycemia, and hyperlipidemia.