Abstract
Objective: To investigate whether patients with behavioral variant frontotemporal dementia (bvFTD) have dysregulation in satiety-related hormonal signaling using a laboratory-based case-control study. Methods: Fifty-four participants (19 patients with bvFTD, 17 patients with Alzheimer disease dementia, and 18 healthy normal controls [NCs]) were recruited from a tertiary-care dementia clinic. During a standardized breakfast, blood was drawn before, during, and after the breakfast protocol to quantify levels of peripheral satiety-related hormones (ghrelin, cortisol, insulin, leptin, and peptide YY) and glucose. To further explore the role of patients' feeding abnormalities on hormone levels, patients were classified into overeating and nonovereating subgroups based on feeding behavior during separate laboratory-based standardized lunch feeding sessions. Results: Irrespective of their feeding behavior in the laboratory, patients with bvFTD, but not patients with Alzheimer disease dementia, have significantly lower levels of ghrelin and cortisol and higher levels of insulin compared with NCs. Furthermore, while laboratory feeding behavior did not predict alterations in levels of ghrelin, cortisol, and insulin, only patients with bvFTD who significantly overate in the laboratory demonstrated significantly higher levels of leptin compared with NCs, suggesting that leptin may be sensitive to particularly severe feeding abnormalities in bvFTD. Conclusions: Despite a tendency to overeat, patients with bvFTD have a hormonal profile that should decrease food intake. Aberrant hormone levels may represent a compensatory response to the behavioral or neuroanatomical abnormalities of bvFTD.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 512-520 |
| Number of pages | 9 |
| Journal | Neurology |
| Volume | 82 |
| Issue number | 6 |
| DOIs | |
| State | Published - Feb 11 2014 |
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ASJC Scopus subject areas
- Clinical Neurology
- Arts and Humanities (miscellaneous)
Cite this
Satiety-related hormonal dysregulation in behavioral variant frontotemporal dementia. / Woolley, Josh D.; Khan, Baber K.; Natesan, Alamelu; Karydas, Anna; Dallman, Mary; Havel, Peter J; Miller, Bruce L.; Rankin, Katherine P.
In: Neurology, Vol. 82, No. 6, 11.02.2014, p. 512-520.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Satiety-related hormonal dysregulation in behavioral variant frontotemporal dementia
AU - Woolley, Josh D.
AU - Khan, Baber K.
AU - Natesan, Alamelu
AU - Karydas, Anna
AU - Dallman, Mary
AU - Havel, Peter J
AU - Miller, Bruce L.
AU - Rankin, Katherine P.
PY - 2014/2/11
Y1 - 2014/2/11
N2 - Objective: To investigate whether patients with behavioral variant frontotemporal dementia (bvFTD) have dysregulation in satiety-related hormonal signaling using a laboratory-based case-control study. Methods: Fifty-four participants (19 patients with bvFTD, 17 patients with Alzheimer disease dementia, and 18 healthy normal controls [NCs]) were recruited from a tertiary-care dementia clinic. During a standardized breakfast, blood was drawn before, during, and after the breakfast protocol to quantify levels of peripheral satiety-related hormones (ghrelin, cortisol, insulin, leptin, and peptide YY) and glucose. To further explore the role of patients' feeding abnormalities on hormone levels, patients were classified into overeating and nonovereating subgroups based on feeding behavior during separate laboratory-based standardized lunch feeding sessions. Results: Irrespective of their feeding behavior in the laboratory, patients with bvFTD, but not patients with Alzheimer disease dementia, have significantly lower levels of ghrelin and cortisol and higher levels of insulin compared with NCs. Furthermore, while laboratory feeding behavior did not predict alterations in levels of ghrelin, cortisol, and insulin, only patients with bvFTD who significantly overate in the laboratory demonstrated significantly higher levels of leptin compared with NCs, suggesting that leptin may be sensitive to particularly severe feeding abnormalities in bvFTD. Conclusions: Despite a tendency to overeat, patients with bvFTD have a hormonal profile that should decrease food intake. Aberrant hormone levels may represent a compensatory response to the behavioral or neuroanatomical abnormalities of bvFTD.
AB - Objective: To investigate whether patients with behavioral variant frontotemporal dementia (bvFTD) have dysregulation in satiety-related hormonal signaling using a laboratory-based case-control study. Methods: Fifty-four participants (19 patients with bvFTD, 17 patients with Alzheimer disease dementia, and 18 healthy normal controls [NCs]) were recruited from a tertiary-care dementia clinic. During a standardized breakfast, blood was drawn before, during, and after the breakfast protocol to quantify levels of peripheral satiety-related hormones (ghrelin, cortisol, insulin, leptin, and peptide YY) and glucose. To further explore the role of patients' feeding abnormalities on hormone levels, patients were classified into overeating and nonovereating subgroups based on feeding behavior during separate laboratory-based standardized lunch feeding sessions. Results: Irrespective of their feeding behavior in the laboratory, patients with bvFTD, but not patients with Alzheimer disease dementia, have significantly lower levels of ghrelin and cortisol and higher levels of insulin compared with NCs. Furthermore, while laboratory feeding behavior did not predict alterations in levels of ghrelin, cortisol, and insulin, only patients with bvFTD who significantly overate in the laboratory demonstrated significantly higher levels of leptin compared with NCs, suggesting that leptin may be sensitive to particularly severe feeding abnormalities in bvFTD. Conclusions: Despite a tendency to overeat, patients with bvFTD have a hormonal profile that should decrease food intake. Aberrant hormone levels may represent a compensatory response to the behavioral or neuroanatomical abnormalities of bvFTD.
UR - http://www.scopus.com/inward/record.url?scp=84895771601&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84895771601&partnerID=8YFLogxK
U2 - 10.1212/WNL.0000000000000106
DO - 10.1212/WNL.0000000000000106
M3 - Article
C2 - 24415571
AN - SCOPUS:84895771601
VL - 82
SP - 512
EP - 520
JO - Neurology
JF - Neurology
SN - 0028-3878
IS - 6
ER -