Effect of lactate and palmitate on substrate utilization of isolated rat soleus

Pearce, Frederick J.; Connett, R. J.

doi:10.1152/ajpcell.1980.238.5.c149

Cited by 46 publications

(25 citation statements)

References 25 publications

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“…In keeping with this notion, the glucose-fatty acid cycle has been demonstrated in brain , mammary tissue (Hawkins & Williamson, 1972;Williamson et al, 1974;Robinson & Williamson, 1977) and submaxillary glands (Thompson & Williamson, 1975), all of which have high rates of glycolysis and glucose oxidation. Likewise it has been observed in the incubated soleus (Maizels et al, 1977;Pearce & Connett, 1980), which, unlike perfused muscle, has a high rate of glycolysis. More direct evidence for the role of glycolysis was presented by Ruderman et al (1978), who found that acetoacetate failed to increase citrate in the incubated soleus when the glycolytic rate was diminished by omitting glucose from the medium.…”

supporting

confidence: 56%

“…Effects of sampling method on muscle metabolite and glycogen contents Earlier studies suggest that the glucose-fatty acid cycle operates in fast-twitch and slow-twitch red muscle, but not in white muscle (Rennie et al, 1976;Maizels et al, 1977;Pearce & Connett, 1980). Some fast-twitch red muscles such as the red portion of the gastrocnemius have to be excised before freeze-clamping.…”

Section: Resultsmentioning

confidence: 99%

“…Initial studies suggested that lipid fuels do not inhibit glucose utilization in incubated or perfused muscle (Beatty & Bocek, 1971;Jefferson et al, 1972;Goodman et al, 1974;Reimer et al, 1975;Berger et al, 1976), with the possible exception of diaphragm (reviewed by Ruderman et al, 1969), but that they inhibit glucose oxidation at the pyruvate dehydrogenase step (Berger et al, 1976;Hagg et al, 1976). More recently, inhibition of glucose utilization and glycolysis by fatty acids and ketone bodies has been demonstrated in rat soleus muscles incubated in vitro (Maizels et al, 1977;Pearce & Connett, 1980); however, contradictory findings have been reported in the isolated perfused, well-oxygenated, rat hindquarter Ruderman et al, 1980;Richter et al, 1982b). Likewise, Rennie et al (1976) have observed increased [citrate] and a lesser degree of glycogen depletion in red muscles of the rat after treadmill exercise in vivo, when plasma non-esterified fatty acid concentrations had been artificially raised.…”

Section: Introductionmentioning

confidence: 99%

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Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Zorzano¹,

Balon²,

Brady³

et al. 1985

Biochemical Journal

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1. Concentrations of citrate, hexose phosphates and glycogen were measured in skeletal muscle and heart under conditions in which plasma non-esterified fatty acids and ketone bodies were physiologically increased. The aim was to determine under what conditions the glucose-fatty acid cycle might be operative in skeletal muscle in vivo. 2. In keeping with the findings of others, starvation increased the concentrations of glycogen, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in heart, indicating that the cycle was operative. In contrast, it decreased glycogen and had no effect on the concentration of citrate or the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in the soleus, a slow-twitch red muscle in which the glucose-fatty acid cycle has been demonstrated in vitro. 3. In fed rats, exercise of moderate intensity caused glycogen depletion in the soleus and red portion of gastrocnemius muscle, but not in heart. In starved rats the same exercise had no effect on the already diminished glycogen contents in skeletal muscle, but it decreased cardiac glycogen by 2530% . 4. After exercise, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio were increased in the soleus of the starved rat. Significant changes were not observed in fed rats. 5. The data suggest that in the resting state the glucose-fatty acid cycle operates in the heart, but not in the soleus muscle, of a starved rat. In contrast, the metabolite profile in the soleus was consistent with activation of the glucose-fatty acid cycle in the starved rat during the recovery period after exercise. Whether the cycle operates during exercise itself is unclear.

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confidence: 56%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Zorzano¹,

Balon²,

Brady³

et al. 1985

Biochemical Journal

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“…Indeed, it has been demonstrated that glycerol kinase (EC 2.7.1.30) is present in human skeletal muscle (Seltzer et al 1989), which suggests the possibility that glycerol may be metabolized. Moreover, glycerol dehydrogenase (EC 1.1.1.6) is also present in human skeletal muscle (Toews, 1966;Hagenfeldt & Wahren, 1968), thus allowing the potential for glycerol to be oxidized (Hagenfeldt & Wahren, 1968;Pearce & Connett, 1980). In summary, it is not critical whether the blood flow to the leg is measured as the arterial inflow or femoral outflow.…”

Section: Arterial-femoral Venous Difference For Substrates and Metabomentioning

confidence: 99%

Skeletal muscle substrate metabolism during exercise: methodological considerations

González‐Alonso

Sacchetti³

et al. 1999

Proc. Nutr. Soc.

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fax +45 3545 7634, email cmrc@rh.dkThe aim of the present article is to evaluate critically the various methods employed in studies designed to quantify precisely skeletal muscle substrate utilization during exercise. In general, the pattern of substrate utilization during exercise can be described well from O 2 uptake measurements and the respiratory exchange ratio. However, if the aim is to quantify limb or muscle metabolism, invasive measurements have to be carried out, such as the determination of blood flow, arterio-venous (a-v) difference measurements for O 2 and relevant substrates, and biopsies of the active muscle. As many substrates and metabolites may be both taken up and released by muscle at rest and during exercise, isotopes can be used to determine uptake and/or release and also fractional uptake can be accounted for. Furthermore, the use of isotopes opens up further possibilities for the estimation of oxidation rates of various substrates. There are several methodological concerns to be aware of when studying the metabolic response to exercise in human subjects. These concerns include: (1) the muscle mass involved in the exercise is largely unknown (bicycle or treadmill). Moreover, whether the muscle sample obtained from a limb muscle and the substrate and metabolite concentrations are representative can be a problem; (2) the placement of the venous catheter can be critical, and it should be secured so that the blood sample represents blood from the active muscle with a minimum of contamination from other muscles and tissues; (3) the use of net limb glycerol release to estimate lipolysis is probably not valid (triacylglycerol utilization by muscle), since glycerol can be metabolized in skeletal muscle; (4) the precision of blood-borne substrate concentrations during exercise measured by a-v difference is hampered since they become very small due to the high blood flow. Recommendations are given in order to obtain more quantitative and conclusive data in studies investigating the regulatory mechanisms for substrate choice by muscle. Free fatty acids: Triacylglycerols: Exercise: Metabolic rate: Respiratory exchange ratioThrough the years, many approaches have been used to evaluate the contribution of carbohydrate and lipids to the increased energy requirements of skeletal muscle during exercise. Since both substrates are stored in the human body outside as well as within the muscle, another question is to what extent the intra-and extra-muscular substrate sources are utilized as a function of exercise intensity, work duration and substrate availability. Determination of the respiratory exchange ratio (RER) from the gas exchange in the lungs or the RQ from the arterial and venous concentration of blood gases can give quite a precise value for the relative contribution of carbohydrates and lipids at the whole-body level or over a limb. To determine the utilization of blood-borne substrates, i.e. the contribution of extramuscular sources, arterio-venous (a-v) differences for relevant substrates and me...

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“…Accordingly, subcutaneous microdialysis in situ (17,18) and cannulation of epigastric veins of the abdominal wall (19) demonstrated that adipose tissue was a significant lactate producer, confirming earlier observations made in vitro (20,21). An intriguing possibility may be that an accelerated lactate flux from the adipose organ enhances gluconeogenesis in the liver (22), decreases glucose uptake in skeletal muscle (23), and promotes insulin secretion (24)-effects that partly explain the metabolic defects reported in the relatives of type 2 diabetic patients.…”

mentioning

confidence: 99%

Increased Lactate Release per Fat Cell in Normoglycemic First-Degree Relatives of Individuals With Type 2 Diabetes

2001

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The aim of this study was to examine subcutaneous lactate production in the relatives of individuals with type 2 diabetes. Therefore, we recruited seven healthy first-degree relatives of type 2 diabetic patients and seven pairwise, matched, healthy control subjects without any heredity for diabetes. All subjects were studied with a euglycemic insulin clamp at ϳ600 pmol/l, abdominal subcutaneous microdialysis, and 133 Xe clearance. Furthermore, a subcutaneous needle biopsy was performed to determine fat cell size. In the fasting state, interstitial lactate was 40% higher in relatives than in control subjects (P ‫؍‬ 0.043), but net lactate production was similar in both groups. However, during the insulin clamp, interstitial lactate (2.50 ؎ 0.29 vs. 1.98 ؎ 0.26 mmol/l, P ‫؍‬ 0.018), interstitial-arterial lactate concentration difference (1.08 ؎ 0.30 vs. 0.53 ؎ 0.24 mmol/l, P ‫؍‬ 0.028), and net lactate release per fat cell (10.9 ؎ 3.7 vs. 2.8 ؎ 1.3 fmol ⅐ cell -1 ⅐ min -1 , P ‫؍‬ 0.018) were increased in the relatives. We conclude that first-degree relatives of type 2 diabetic patients may have an enhanced net lactate release per fat cell in abdominal subcutaneous tissue. This could suggest a pathological regulation in adipose tissue that is of importance for the metabolic defects known in type 2 diabetic relatives.

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Effect of lactate and palmitate on substrate utilization of isolated rat soleus

Cited by 46 publications

References 25 publications

Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Skeletal muscle substrate metabolism during exercise: methodological considerations

Increased Lactate Release per Fat Cell in Normoglycemic First-Degree Relatives of Individuals With Type 2 Diabetes

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