# Lesions involving the insula are associated with reduced appetite and weight loss

**Authors:** Wanzhi Lyu, Joel Bruss, Emily R Dappen, Joseph C Griffis, Benjamin Pace, Brandon Neisewander, Kenneth Manzel, Daniel Tranel, Aaron D Boes, Nicholas T Trapp

PMC · DOI: 10.1093/braincomms/fcag044 · Brain Communications · 2026-02-25

## TL;DR

Brain damage in the right posterior insula is linked to reduced appetite and weight loss, offering new insights into how the brain regulates eating and weight.

## Contribution

Lesions in the right posterior insula are newly identified as key to appetite and weight regulation.

## Key findings

- Lesions in the right posterior insula are associated with decreased appetite.
- Damage to this region correlates with significant weight loss.
- The insula plays a role in higher-order appetite regulation.

## Abstract

Eating-related disorders such as anorexia nervosa, bulimia nervosa and obesity are associated with high rates of morbidity and mortality in the United States. To investigate the neuroanatomical structures involved in appetite and weight change, we employed lesion symptom mapping. 358 patients with focal brain lesions and appetite ratings were recruited, as well as 48 patients with pre- and post-lesion weight records. Partial least squares regression identified a significant association between patterns of brain damage and appetite change (model R2 = 0.13, P = 0.006), and the relationship between lesion location and weight change was explored using the proportional subtraction method. The right posterior insula was the peak region associated with both decreased appetite and weight loss, providing new insight into the neural correlates of higher-order appetite regulation and weight management.

Lyu et al. demonstrated that damage to specific brain regions relates to changes in appetite and weight after neurological injury. In two distinct analyses, lesions to the right posterior insula were associated with reduced appetite and weight loss, identifying this region as a key contributor to appetite and weight regulation.

Graphical Abstract

## Linked entities

- **Diseases:** anorexia nervosa (MONDO:0005351), bulimia nervosa (MONDO:0005452), obesity (MONDO:0011122)

## Full-text entities

- **Diseases:** under- or over-eating (MESH:D006963), fatigue (MESH:D005221), dysarthric speech (MESH:D004401), insular dysfunction (MESH:D006331), Eating-related disorders (MESH:D001068), Stroke (MESH:D020521), anorexia nervosa (MESH:D000856), weight gain (MESH:D015430), mood disorder (MESH:D019964), Depression (MESH:D003866), obese (MESH:D009765), Lesions (MESH:D009059), Disorders (MESH:D009358), basal ganglia lesion (MESH:D001480), insula damage (MESH:D020263), functional impairment (MESH:D003072), anxiety disorders (MESH:D001008), Motor impairment (MESH:D000068079), upper and lower extremity weakness (MESH:D020335), bulimia nervosa (MESH:D052018), neurologic disorders (MESH:D009461), major depressive disorder (MESH:D003865), increased (MESH:D000067251), caloric restriction (MESH:D002313), brain injury (MESH:D001930), brain lesion (MESH:D001927), neurological injury (MESH:D020196), brain damage (MESH:D001925), reduced mobility (MESH:D014086), haemorrhagic stroke (MESH:D002543), subarachnoid haemorrhage (MESH:D013345), decrease (MESH:D009123), craving (MESH:C564883), binge eating disorder (MESH:D056912), epilepsy (MESH:D004827), loss (MESH:D016388), taste and eating dysfunction (MESH:D013651), binge eating (MESH:D002032), appetite and weight loss (MESH:D015431), traumatic brain injury (MESH:D000070642), insula, caudate and putamen lesion (MESH:D020146), striatum dysfunction (MESH:D020267), anxiety (MESH:D001007), anorexia (MESH:D000855), alcohol or drug abuse (MESH:D019966), irritability (MESH:D001523), psychosis (MESH:D011618), ischaemic stroke (MESH:D002544), motor weakness (MESH:D018908)
- **Chemicals:** dopamine (MESH:D004298), nicotine (MESH:D009538)
- **Species:** Nicotiana tabacum (American tobacco, species) [taxon 4097], Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

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## References

64 references — full list in the complete paper: https://tomesphere.com/paper/PMC12933212/full.md

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Source: https://tomesphere.com/paper/PMC12933212