Insulin Resistance of Stress: Sites and Mechanisms

Brandi, L. S.; Santoro, D; Natali, Andrea; Altomonte, F; Baldi, Simona; Frascerra, Silvia; Ferrannini, Eleuterio

doi:10.1042/cs0850525

Cited by 55 publications

(35 citation statements)

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“…Thus, in deep forearm tissues the peak effect of insulin was to promote the uptake of 3 ymol min ' of glucose per each 10 ,umol min -' of oxygen regardless of blood flow. For comparison, in eight age-matched insulin sensitive subjects receiving an insulin infusion of the same duration and dose (28), the glucose to oxygen ratio in the forearm was 0.65±+0.23, i.e., more than twofold higher (P < 0.01) than in the present hypertensive subjects. The implication of these results is that the insulin resistance of essential hypertension is predominantly a cellular phenomenon rather than a restriction in insulin and glucose delivery to muscle tissue.…”

Section: Discussionmentioning

confidence: 93%

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

Natali

Bonadonna²,

Santoro³

et al. 1994

J. Clin. Invest.

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IntroductionInsulin-mediated vasodilation has been proposed as a determinant of in vivo insulin sensitivity. We tested whether sustained vasodilation with adenosine could overcome the muscle insulin resistance present in mildly overweight patients with essential hypertension. Using the forearm technique, we measured the response to a 40-min local intraarterial infusion of adenosine given under fasting conditions (n = 6) or superimposed on a euglycemic insulin clamp (n = 8). In the fasting state, adenosine-induced vasodilation (forearm blood flow from 2.6+0.6 to 6.0±+1.2 ml min-'dl-', P < 0.001) was associated with a 45% rise in muscle oxygen consumption (5.9+1.0 vs 8.6+1.7 amol min'-dl-', P < 0.05), and a doubling of forearm glucose uptake (0.47+0.15 to 1.01+0.28 ,Amol min'-dl'-, P < 0.05). The latter effect remained significant also when expressed as a ratio to concomitant oxygen balance (0.08±0.03 vs 0.13+0.04 jAmol tumol'-, P < 0.05), whereas for all other metabolites (lactate, pyruvate, FFA, glycerol, citrate, and 13-hydroxybutyrate) this ratio remained unchanged.During euglycemic hyperinsulinemia, whole-body glucose disposal was stimulated (to 19+3 jmol min-'kg-'), but forearm blood flow did not increase significantly above baseline (2.9+0.2 vs 3.1+0.2 ml min'-dl'`, P = NS). Forearm oxygen balance increased (by 30%, P < 0.05) and forearm glucose uptake rose fourfold (from 0.5 to 2.3 Amol min-'dl-', P < 0.05). Superimposing an adenosine infusion into one forearm resulted in a 100% increase in blood flow (from 2.9+0.2 to 6.1+0.9 ml min-'dl-', P < 0.001); there was, however, no further stimulation of oxygen or glucose uptake compared with the control forearm. During the clamp, the ratio of glucose to oxygen uptake was similar in the control and in the infused forearms (0.27±0.11 and 0.23+0.09, respectively), and was not altered by adenosine (0.31±0.9 and 0.29+0.10). We conclude that in insulin-rel5-76sistant patients with hypertension, adenosine-induced vasodilation recruits oxidative muscle tissues and exerts a modest, direct metabolic effect to promote muscle glucose uptake in the fasting state. Despite these effects, however, adenosine does not overcome muscle insulin resistance. (J. Clin. Invest. 1994. 94:1570-1576 (3)(4)(5). The role of blood flow, and, consequently, of the supply of glucose and insulin to target tissues in the physiologic modulation of in vivo glucose metabolism has been recently reevaluated. Evidence has been provided that systemic insulin infusion with maintenance of euglycemia is associated with peripheral vasodilation (6). When regional data have been extrapolated to the whole body, the insulin-induced increase in blood flow has been estimated to explain up to 50% of the total amount of glucose taken by skeletal muscle (7). Furthermore, typical states of insulin resistance, such as obesity and diabetes mellitus, have been reported to manifest both cellular (i.e., reduced arterio-venous gradient) and vascular (i.e., blunted vasodilation) resistance to insulin action (7,8). Thus, the ...

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Section: Discussionmentioning

confidence: 93%

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

Natali

Bonadonna²,

Santoro³

et al. 1994

J. Clin. Invest.

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“…Například někteří autoři se domnívají, že schopnost oxidovat glukózu je u septických pacientů vyšší při porovnání se zdravými dobrovolníky (71), zatímco jiní tvrdí, že je nižší (72-74) nebo se nemění (66,75). Brandi dokumentoval, že celotělová oxidace glukózy probíhá preferenčně v játrech a jiných tkáních než svalových (76). Zároveň i na úrovni jednotlivých svalů a zastoupení typů svalových vláken se oxidace liší (77,78).…”

Section: Skořepa a Kol: úStřední Role Glukózy V Metabolismu A Výživěunclassified

The Central Role of Glucose in Metabolism and Nutrition of Critically Ill Patients

Skořepa¹,

Sobotka²,

Fortunato³

et al. 2017

Mil. Med. Sci. Lett.

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“…As shown by studies in experimental animals and in man, post absorbtive glucose production (sustained by the liver and to a lesser extent by the kidneys [5]) is regulated by plasma glucose concentration itself [4] insulin and counterregulatory hormones (mainly glucagon and adrenaline) [6]. Case control studies have shown that in the postabsorptive state diabetic patients in poor metabolic control [2] and severely stressed people [7] have an increased rate of endogenous glucose output (EGO), which is almost invariably associated with a reduced plasma glucose clearance and, therefore, hyperglycaemia. Due to the technical difficulty of using tracers in large groups of subjects, the physiologic determinants, the normal values and the true degree of inter-individual variability of postabsorptive EGO have, however, not been determined.…”

Section: : 1266±1272]mentioning

confidence: 99%

Determinants of postabsorptive endogenous glucose output in non-diabetic subjects

Natali

Toschi²,

Camastra³

et al. 2000

Diabetologia

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IntroductionIn non-diabetic subjects, fasting plasma glucose concentrations are maintained stable through a fine balance between glucose utilisation by body tissues and endogenous glucose release. Different laboratories [1±4] have reported (mostly in small groups of subjects) that, in euglycaemic subjects after an overnight fast endogenous glucose utilisation averages 9±12 mmol´min ±1 per kg of body weight, with a rather limited inter-individual variability (20±30 %). In a 75-kg man, therefore, approximately 9 g of glucose Diabetologia (2000) , range 209±1512) and was strongly related to lean body mass (r = 0.63, p < 0.0001). This association entirely explained the endogenous glucose output being higher in men than in women (827 189 vs 674 187 mmol min ±1 , p < 0.0001), its relation to body mass (+ 10 2 per unit of body mass index, p < 0.0001) and its trend to decline with age (±1.1 0.7 mmol´min ±1 per year, p = 0.10). Although inversely related to one another (r = ±0.41, p < 0.0001), peripheral insulin sensitivity and fasting plasma insulin were both independently associated with endogenous glucose output in an inverse fashion (with partial r's of 0.19 and 0.21, respectively, after adjusting for lean body mass and centre, p < 0.0001 for both). Conclusion/interpretation. Among non-diabetic subjects in the postabsorptive condition, total body endogenous glucose output variability is wide and is largely explained by the amount of lean mass; this, in turn, explains differences in total endogenous glucose output due to sex, obesity and age. Independently of the amount of lean mass, peripheral insulin resistance is associated with a higher endogenous glucose output independently of fasting plasma insulin concentration, suggesting coupled regulation of insulin action in peripheral tissues and the liver. [Diabetologia (2000)

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Insulin Resistance of Stress: Sites and Mechanisms

Cited by 55 publications

References 0 publications

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

The Central Role of Glucose in Metabolism and Nutrition of Critically Ill Patients

Determinants of postabsorptive endogenous glucose output in non-diabetic subjects

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