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The lateral hypothalamus: A site for integration of nutrient and fluid balance
van Dijk, G., Evers, S. S., Guidotti, S., Thornton, S. N., Scheurink, A. J. W. & Nyakas, C., 10-Aug-2011, In : Behavioral Brain Research. 221, 2, p. 481-487 7 p.Research output: Contribution to journal › Review article › Academic › peer-review
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The lateral hypothalamus : A site for integration of nutrient and fluid balance. / van Dijk, Gertjan; Evers, Simon S.; Guidotti, Stefano; Thornton, Simon N.; Scheurink, Anton J. W.; Nyakas, Csaba.
In: Behavioral Brain Research, Vol. 221, No. 2, 10.08.2011, p. 481-487.Research output: Contribution to journal › Review article › Academic › peer-review
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TY - JOUR
T1 - The lateral hypothalamus
T2 - A site for integration of nutrient and fluid balance
AU - van Dijk, Gertjan
AU - Evers, Simon S.
AU - Guidotti, Stefano
AU - Thornton, Simon N.
AU - Scheurink, Anton J. W.
AU - Nyakas, Csaba
PY - 2011/8/10
Y1 - 2011/8/10
N2 - This paper reviews seemingly obligatory relations between nutrient and fluid balance. A relatively novel neuronal pathway involving interplay between acetylcholine and the melanocortins, alpha MSH and AGRP in the arcuate nucleus (Arc) of the hypothalamus projecting to the lateral hypothalamus (LH) may bridge this gap. In the fasted condition, increased expression of MCH (due to muscarinic-3 receptor stimulation and low melanocortin tone) and neuronal release of MCH (via Orexin signaling) underlies a drive towards positive energy balance, increased B cell capacity to secrete insulin, and this is associated with optimal fluid homeostasis. A hypohydrated state is hypothesized to yield downregulation of leptin signaling (potentially via inhibitory effects of osmotic stress on mTOR), but osmotic stress may prevent MCH expression via the OVLT-SFO complex. If this occurs in an obese state, impaired pancreatic B cell capacity and peripheral insulin insensitivity as a result of hypohydration may underlie cardio-metabolic diseases. (C) 2011 Elsevier B.V. All rights reserved.
AB - This paper reviews seemingly obligatory relations between nutrient and fluid balance. A relatively novel neuronal pathway involving interplay between acetylcholine and the melanocortins, alpha MSH and AGRP in the arcuate nucleus (Arc) of the hypothalamus projecting to the lateral hypothalamus (LH) may bridge this gap. In the fasted condition, increased expression of MCH (due to muscarinic-3 receptor stimulation and low melanocortin tone) and neuronal release of MCH (via Orexin signaling) underlies a drive towards positive energy balance, increased B cell capacity to secrete insulin, and this is associated with optimal fluid homeostasis. A hypohydrated state is hypothesized to yield downregulation of leptin signaling (potentially via inhibitory effects of osmotic stress on mTOR), but osmotic stress may prevent MCH expression via the OVLT-SFO complex. If this occurs in an obese state, impaired pancreatic B cell capacity and peripheral insulin insensitivity as a result of hypohydration may underlie cardio-metabolic diseases. (C) 2011 Elsevier B.V. All rights reserved.
KW - Body water
KW - Drinking
KW - Feeding
KW - Osmotic stress
KW - Obesity
KW - Insulin
KW - MELANIN-CONCENTRATING HORMONE
KW - IBOTENIC ACID LESIONS
KW - METHYL-D-ASPARTATE
KW - FOOD-INTAKE
KW - BODY-WEIGHT
KW - CHOLINERGIC STIMULATION
KW - SUBFORNICAL ORGAN
KW - ARCUATE NUCLEUS
KW - ACETYLCHOLINE-RELEASE
KW - DEHYDRATION ANOREXIA
U2 - 10.1016/j.bbr.2011.01.047
DO - 10.1016/j.bbr.2011.01.047
M3 - Review article
VL - 221
SP - 481
EP - 487
JO - Behavioral Brain Research
JF - Behavioral Brain Research
SN - 0166-4328
IS - 2
ER -
ID: 5340844