Untersuchungen zum muskulären Kohlenhydrat- und Fettstoffwechsel am Modell des hämoglobinfrei perfundierten Rattenhinterbeins

Reimer, F; Löffler, Georg; Wieland, O.

doi:10.1007/978-3-642-85449-1_363

Cited by 3 publications

(6 citation statements)

References 6 publications

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“…However, the same was found in some in vitro-investigations which demonstrated a lack of hormonal stimulation and rather a substrate-stimulation (Reimer et al 1973;Rosen et al 1981;Standi et al 1980). It should be noted that the intraarterially infused dosage of insulin did not stimulate glucose uptake of resting skeletal muscle.…”

Section: Discussionmentioning

confidence: 55%

“…Some intermediates of the glycolytic pathway could be discussed since it is known that the rate of muscular reesteriflcation is stimulated by increasing intracellular levels of a-glycero-phosphate (Reimer et al 1973). Seen from a more teleological view it seems quite obvious that the muscular rate of lipolysis is not regulated systemically by hormones but rather locally by substrate supply.…”

Section: Discussionmentioning

confidence: 99%

“…However, there are some data from in vitro and in vivo experiments which are not consistent with this notion: hormonal regulation of triglyceride-synthesis and -degradation could not be found, or was not sensitive, respectively {Garland and Randle 1963; Jato-Rodriguez, Hudson and Strickland 1974;Reimer, Loffler, Gerbitz and Wieland 1973;Rosen, Ubrig, Adrian, Feuerstein and Reinauer 1981). On the other hand, substrate-regulation according to a supply-stimulation and product-inhibition seemed possible (Reimer et al 1973;Rosen et al 1981;Standl, Lotz, Dexel, Janka and Kolb 1980). In order to yield further information regarding triglyceride metabolism in muscle tissue, we have studied the release of glycerol from skeletal muscle …”

Section: Introductionmentioning

confidence: 87%

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Evidence for a Substrate Regulation of Triglyceride Lipolysis in Human Skeletal Muscle

Wicklmayr¹,

Dietze²,

Rett³

et al. 1985

Horm Metab Res

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Glycerol release from the human forearm which is generally used as a semiquantitative index of intramuscular lipolysis was studied under different hormonal influence and substrate supply in healthy volunteers and juvenile diabetics using the forearm technique. Acute insulin deficiency in juvenile diabetics failed stimulating the rate of muscular lipolysis since the rates of glycerol release in normals and diabetics were the same. In addition, in normal volunteers high physiological levels of insulin caused by an intraarterial infusion of the hormone exhibited no effect on the glycerol release from deep forearm tissue. Similarly, an intraarterial infusion of metaproterenol did not accelerate muscular glycerol release in normal man. However, in juvenile diabetics in acute insulin deficiency the same dose of the catecholamine increased the rate of muscular glycerol production. Elevated substrate supply during intravenous infusion of glucose or fructose yielded increased uptake of glucose and fructose into the deep forearm tissue and thereby promptly blocked muscular glycerol release in normal volunteers and in juvenile diabetics. These findings suggest that the rate of lipolysis in muscle tissue is not primarily under the control of hormones but rather by substrate supply.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 87%

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Evidence for a Substrate Regulation of Triglyceride Lipolysis in Human Skeletal Muscle

Wicklmayr¹,

Dietze²,

Rett³

et al. 1985

Horm Metab Res

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“…Only a few studies however have focussed on the regulation of synthesis and degradation of intramuscular triglycerides. According to sporadic data, the latter does not seem to be primarily controlled by hormones under physiological conditions {Garland and Randle 1963; Jato-Rodriguez, Hudson and Strickland 1974;Reimer, Loffler, Gerbitz and Wieland 1973;Rosen, Ubrig, Adrian, Feuerstein and Reinauer 1981;Wicklmayr, Dietze, Rett and Mehnert 1985), but might rather be subject to a demand-regulation which is modulated by substrate supply {Reimer et al 1913;Rosen et al 1981;Standi, Lotz, Drexel, Janka and Kolb 1980), as it has been shown for glucose and fructose {Wicklmayr et al 1985). The present study was performed in order to investigate whether ketone bodies may also influence muscular triglyceride lipolysis in vivo.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Muscular Triglyceride Lipolysis by Ketone Bodies: A Mechanism for Energy-Preservation in Starvation

Wicklmayr¹,

Rett²,

Dietze³

et al. 1986

Horm Metab Res

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Using the forearm technique, muscle substrate balances were measured in healthy volunteers under the influence of a low dose intraarterial infusion of beta-hydroxybutyrate. The ketone body led to a prompt cessation of muscular release of glycerol and free fatty acids, indicating inhibited muscular triglyceride lipolysis. This finding confirms the concept of substrate regulation of muscle triglyceride lipolysis in vivo.

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“…In both adductormuscle fibres of the rhesus monkey (Beatty & Bocek, 1971) and the isolated perfused rat hindquarter (Houghton-& Ruderman, 1971;Jefferson, et al, 1972; at., 11974; Reimer et al, 1974), exogenous fatty acids and ketone bodies do not inhibit insulin-stimulated glucose uptake. Further, the characteristic changes in tissue glycogen, citrate and hexose monophosphates noted in hearts of starved and diabetic rats are not seen in skeletal muscle (Adrouny, 1969;Goodman et al, 1974).…”

mentioning

confidence: 98%

Glucose metabolism in perfused skeletal muscle. Effects of starvation, diabetes, fatty acids, acetoacetate, insulin and exercise on glucose uptake and disposition

Berger¹,

Hagg²,

Goodman³

et al. 1976

Biochemical Journal

183

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1. The regulation of glucose uptake and disposition in skeletal muscle was studied in the isolated perfused rat hindquarter. 2. Insulin and exercise, induced by sciatic-nerve stimulation, enhanced glucose uptake about tenfold in fed and starved rats, but were without effect in rats with diabetic ketoacidosis. 3. At rest, the oxidation of lactate (0.44,umol/ mi per 30g ofmuscle in fed-rats) was decreased by 75% in both starved and diabetic rats, whereas the release of alanine and lactate (0.41 and 1.35,umol/min per 30g respectively in the fed state) was increased. Glycolysis, defined as the sum of lactate+alanine release and lactate oxidation, was not decreased in either starvation or diabetes. 4. In all groups, exercise tripled 02 consumption (from -8 to -25umol/min per 30g of muscle) and increased the release and oxidation of lactate five-to ten-fold. The differences in lactate release between fed, starved and diabetic rats observed at rest were no longer apparent however, lactate oxidation was still several times greater in the fed group. 5. Perfusion of the hindquarter ofa fed rat with palmitate, octanoate or acetoacetate did not alter glucose uptake or lactate release in either resting or exercising muscle; however, lactate oxidation was significantly inhibited by acetoacetate, which also increased the intracellular concentration of acetyl-CoA. 6. The data suggest that neither glycolysis nor the capacity for glucose transport are inhibited in the perfused hindquarter during starvation or perfusion with fatty acids or ketone bodies. On the other hand, lactate oxidat-ion is inhibited, suggesting diminished activity ofpyruvate dehydrogenase. 7. Differences in the regulation of glucose metabolism in heart and skeletal muscle and the role of the glucose/fatty acid cycle in each tissue are discussed.The present paper deals with the alterations in muscle-glucose metabolism that occur in starvation and diabetes and therole offreefatty acids and ketone bodies in causing these changes. Much of our present knowledge of this subject has been derived from experiments carried out in the perfused rat heart. Using this preparation, Randle et al. (1966) observed an inhibition of the tiptake, phosphorylation and oxidation of glucose and a -block in glycolysis at the level-of phosphofructokitase both in starvation and diabetes. In iddition, they obsrved a similar pattern in hearts perfused with fatty acids and ketone bodies, whichiled themto stggest that the increased utilization of these substrates in starved and diabetic rats might explain the impaired -glucose metabolism in these states. Comparable findings have been observed in diaphragm by some laboratories but not others (see Ruderman et al., 1969).

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Untersuchungen zum muskulären Kohlenhydrat- und Fettstoffwechsel am Modell des hämoglobinfrei perfundierten Rattenhinterbeins

Cited by 3 publications

References 6 publications

Evidence for a Substrate Regulation of Triglyceride Lipolysis in Human Skeletal Muscle

Evidence for a Substrate Regulation of Triglyceride Lipolysis in Human Skeletal Muscle

Inhibition of Muscular Triglyceride Lipolysis by Ketone Bodies: A Mechanism for Energy-Preservation in Starvation

Glucose metabolism in perfused skeletal muscle. Effects of starvation, diabetes, fatty acids, acetoacetate, insulin and exercise on glucose uptake and disposition

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