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About This Item
Empirical Formula (Hill Notation):
C6H12O5
CAS Number:
Molecular Weight:
164.16
EC Number:
MDL number:
UNSPSC Code:
12352201
PubChem Substance ID:
Pricing and availability is not currently available.
mp
101-103 °C (lit.)
storage temp.
2-8°C
SMILES string
OCC1OC(CO)C(O)C1O
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Storage Class Code
13 - Non Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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R Cermak et al.
Biochimica et biophysica acta, 1421(1), 116-124 (1999-11-16)
The fructose analogue 2,5-anhydro-D-mannitol (2,5-AM), which depletes liver cells of ATP, has been shown to alter liver cell membrane potential (V(m)) in situ and in superfused liver slices. To study this effect of 2,5-AM on hepatocytes in more detail, patch-clamp
H Ji et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 278(6), R1579-R1582 (2000-06-10)
Previous studies indicate that administration of the metabolic inhibitor, 2,5-anhydro-D-mannitol (2,5-AM) or methyl palmoxirate (MP), induces feeding behavior in rats by lowering hepatic energy status. Combined treatment with these agents synergistically increases food intake. The present study was designed to
M I Friedman
The Proceedings of the Nutrition Society, 56(1A), 41-50 (1997-03-01)
Control of energy intake, either in response to changes in the energy content of food or in energy expenditures and storage, is based on the detection of a feedback signal generated in the processing of metabolic fuels for energy. Evidence
E Scharrer et al.
The American journal of physiology, 272(3 Pt 2), R874-R878 (1997-03-01)
Because 2,5-anhydro-D-mannitol (2,5-AM) seems to stimulate feeding by acting on the liver and because the hepatic membrane potential has been suggested to play an important role in control of feeding ("potentiostatic" hypothesis), we investigated the effect of 2,5-AM on the
S Aiston et al.
Diabetologia, 43(5), 589-597 (2000-06-16)
The Zucker fatty fa/fa rat develops hyperinsulinaemia, insulin-resistance and severe obesity as a result of a homozygous mutation in the leptin receptor gene. The aim was to characterise the metabolic defect(s) in hepatocytes from fa/fa rats. Glucose metabolism and key
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