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Glycerol Production from Glucose and Fructose by 3T3-L1 Cells: A Mechanism of Adipocyte Defense from Excess Substrate.

Romero Mdel M, Sabater D, Fernández-López JA, Remesar X, Alemany M - PLoS ONE (2015)

Bottom Line: Fructose conversion to lactate and glycerol was lower than that of glucose.When both hexoses were present, the effects of fructose on gene expression prevailed over those of glucose.A phosphatase pathway such as that described may have a potential regulatory function, and explain the production of glycerol by adipocytes in the absence of lipolytic stimulation.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition and Food Science, Faculty of Biology, University of Barcelona, Av.Diagonal 643, 08028, Barcelona, Spain; Institute of Biomedicine, University of Barcelona, Barcelona, Spain; CIBER Obesity and Nutrition, Barcelona, Spain.

ABSTRACT
Cultured adipocytes (3T3-L1) produce large amounts of 3C fragments; largely lactate, depending on medium glucose levels. Increased glycolysis has been observed also in vivo in different sites of rat white adipose tissue. We investigated whether fructose can substitute glucose as source of lactate, and, especially whether the glycerol released to the medium was of lipolytic or glycolytic origin. Fructose conversion to lactate and glycerol was lower than that of glucose. The fast exhaustion of medium glucose was unrelated to significant changes in lipid storage. Fructose inhibited to a higher degree than glucose the expression of lipogenic enzymes. When both hexoses were present, the effects of fructose on gene expression prevailed over those of glucose. Adipocytes expressed fructokinase, but not aldolase b. Substantive release of glycerol accompanied lactate when fructose was the substrate. The mass of cell triacylglycerol (and its lack of change) could not justify the comparatively higher amount of glycerol released. Consequently, most of this glycerol should be derived from the glycolytic pathway, since its lipolytic origin could not be (quantitatively) sustained. Proportionally (with respect to lactate plus glycerol), more glycerol was produced from fructose than from glucose, which suggests that part of fructose was catabolized by the alternate (hepatic) fructose pathway. Earlier described adipose glycerophophatase activity may help explain the glycolytic origin of most of the glycerol. However, no gene is known for this enzyme in mammals, which suggests that this function may be carried out by one of the known phosphatases in the tissue. Break up of glycerol-3P to yield glycerol, may be a limiting factor for the synthesis of triacylglycerols through control of glycerol-3P availability. A phosphatase pathway such as that described may have a potential regulatory function, and explain the production of glycerol by adipocytes in the absence of lipolytic stimulation.

No MeSH data available.


Related in: MedlinePlus

Glycerol-producing pathways in mammalian adipocytes.The numbers indicate the pathways described in the Discussion: 1: lipolysis (red); 2: reduction of fructose-derived glyceraldehyde (exclusive fructose metabolism: blue); 3: postulated glycerol-3-phosphatase pathway (green).
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pone.0139502.g006: Glycerol-producing pathways in mammalian adipocytes.The numbers indicate the pathways described in the Discussion: 1: lipolysis (red); 2: reduction of fructose-derived glyceraldehyde (exclusive fructose metabolism: blue); 3: postulated glycerol-3-phosphatase pathway (green).

Mentions: Probably, the most critical finding of this study is the quantitatively important release of glycerol by WAT in response to increasing medium hexoses. The net and quantitatively significant release of glycerol to the bloodstream [31], irrespective of its lipolytic or glycolytic origin, provides the liver with an excellent (and non-acidic) gluconeogenic substrate, which is directly incorporated at the triose-P level. Fig 6 shows the three known pathways for the production (and release) of glycerol into the medium by mammalian adipocytes. Path 1 is the best-known, glycerol as a byproduct of lipolysis [32]; there are, however, studies indicating a significant contribution of the glycolytic pathway to the production of glycerol [33].


Glycerol Production from Glucose and Fructose by 3T3-L1 Cells: A Mechanism of Adipocyte Defense from Excess Substrate.

Romero Mdel M, Sabater D, Fernández-López JA, Remesar X, Alemany M - PLoS ONE (2015)

Glycerol-producing pathways in mammalian adipocytes.The numbers indicate the pathways described in the Discussion: 1: lipolysis (red); 2: reduction of fructose-derived glyceraldehyde (exclusive fructose metabolism: blue); 3: postulated glycerol-3-phosphatase pathway (green).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4591265&req=5

pone.0139502.g006: Glycerol-producing pathways in mammalian adipocytes.The numbers indicate the pathways described in the Discussion: 1: lipolysis (red); 2: reduction of fructose-derived glyceraldehyde (exclusive fructose metabolism: blue); 3: postulated glycerol-3-phosphatase pathway (green).
Mentions: Probably, the most critical finding of this study is the quantitatively important release of glycerol by WAT in response to increasing medium hexoses. The net and quantitatively significant release of glycerol to the bloodstream [31], irrespective of its lipolytic or glycolytic origin, provides the liver with an excellent (and non-acidic) gluconeogenic substrate, which is directly incorporated at the triose-P level. Fig 6 shows the three known pathways for the production (and release) of glycerol into the medium by mammalian adipocytes. Path 1 is the best-known, glycerol as a byproduct of lipolysis [32]; there are, however, studies indicating a significant contribution of the glycolytic pathway to the production of glycerol [33].

Bottom Line: Fructose conversion to lactate and glycerol was lower than that of glucose.When both hexoses were present, the effects of fructose on gene expression prevailed over those of glucose.A phosphatase pathway such as that described may have a potential regulatory function, and explain the production of glycerol by adipocytes in the absence of lipolytic stimulation.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition and Food Science, Faculty of Biology, University of Barcelona, Av.Diagonal 643, 08028, Barcelona, Spain; Institute of Biomedicine, University of Barcelona, Barcelona, Spain; CIBER Obesity and Nutrition, Barcelona, Spain.

ABSTRACT
Cultured adipocytes (3T3-L1) produce large amounts of 3C fragments; largely lactate, depending on medium glucose levels. Increased glycolysis has been observed also in vivo in different sites of rat white adipose tissue. We investigated whether fructose can substitute glucose as source of lactate, and, especially whether the glycerol released to the medium was of lipolytic or glycolytic origin. Fructose conversion to lactate and glycerol was lower than that of glucose. The fast exhaustion of medium glucose was unrelated to significant changes in lipid storage. Fructose inhibited to a higher degree than glucose the expression of lipogenic enzymes. When both hexoses were present, the effects of fructose on gene expression prevailed over those of glucose. Adipocytes expressed fructokinase, but not aldolase b. Substantive release of glycerol accompanied lactate when fructose was the substrate. The mass of cell triacylglycerol (and its lack of change) could not justify the comparatively higher amount of glycerol released. Consequently, most of this glycerol should be derived from the glycolytic pathway, since its lipolytic origin could not be (quantitatively) sustained. Proportionally (with respect to lactate plus glycerol), more glycerol was produced from fructose than from glucose, which suggests that part of fructose was catabolized by the alternate (hepatic) fructose pathway. Earlier described adipose glycerophophatase activity may help explain the glycolytic origin of most of the glycerol. However, no gene is known for this enzyme in mammals, which suggests that this function may be carried out by one of the known phosphatases in the tissue. Break up of glycerol-3P to yield glycerol, may be a limiting factor for the synthesis of triacylglycerols through control of glycerol-3P availability. A phosphatase pathway such as that described may have a potential regulatory function, and explain the production of glycerol by adipocytes in the absence of lipolytic stimulation.

No MeSH data available.


Related in: MedlinePlus