Genetic effects on body weight in mice are highly heterogeneous, dynamic, and nonlinear with respect to genomic background, age, and diet.

Taller body height in young adulthood, as marker of early-life environment, is associated with lower risk of dementia diagnosis independently of cognitive reserve and family factors shared among brothers.

Cell type-specific transcriptomics in energy homeostasis neurons has identified hundreds of genes and multiple signaling pathways that are regulated by weight loss in mice, as well as several previously unexamined genes that can regulate appetite and body weight.

In Drosophila melanogaster, nutrition controls body size by acting through the Forkhead Box class O (FoxO)/Ultraspiracle complex to regulate nutrition-sensitive ecdysone biosynthesis, thereby controlling the switch to stop growth.

The preoptic area (POA) regulates distinct metabolic adaptations, via leptin-dependent (fasting-induced hypometabolism and high-fat-diet-induced hypermetabolism), or leptin-independent mechanisms (temperature induced metabolic changes) and thus significantly contributes to body weight homeostasis.

RAI1 regulates molecular signalling and intrinsic excitability of hypothalamic brain-derived neurotrophic factor neurons important for energy homeostasis.

A novel and distinct cholecystokinin brain circuit critically modulates food intake and body weight.

The Acyl-CoA binding domain-containing 7 (Acbd7) gene is expressed in the hypothalamus, encodes a peptide that suppresses appetite, increases metabolic rate and interacts with the leptin-melanocortin system.

It is unclear how much a child's BMI at age 8 affects their depressive and ADHD symptoms after family-level factors are accounted for, but a substantial impact on anxiety symptoms is unlikely.

Genetic interaction and biochemical analyses have unveiled the crucial involvement of CTPS in the regulation of adipocyte growth, lipid metabolism, and metabolic adaptation in Drosophila, achieved through activating the PI3K-Akt-SREBP pathway.