Hypoglycemia, brain metabolism, and brain damage

Siesjö, Bo K.

doi:10.1002/dmr.5610040203

Cited by 117 publications

(39 citation statements)

References 123 publications

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“…Thus, in the present study it is likely that the splanchnic tissues contributed to increase total body glucose uptake. Since, however, the splanchnic tissues only take up glucose in proportion to the prevailing plasma glucose concentration [2,21,39] and since net brain glucose uptake is not enhanced by hyperglycaemia [37,38], from a quantitative standpoint it is clear that peripheral tissues (muscle) were responsible for a significant proportion of glucose disposal. Consistent with this, Baron et al [36] have shown that the majority of total body glucose uptake in response to insulinopenic hyperglycaemia occurs in muscle.…”

Section: Discussionmentioning

confidence: 99%

“…In the postabsorptive state, when the plasma insulin concentration is at basal levels, the majority of glucose uptake occurs in insulin-insensitive tissues, mainly the brain and the splanchnic organs [36]. Glucose utilization by the central nervous system is saturated at plasma glucose concentrations over 3.3 mmol/l [37,38], whereas, in the presence of basal insulin levels, splanchnic glucose uptake augments in proportion to the degree of hyperglycaemia [2,21,39]. Thus, in the present study it is likely that the splanchnic tissues contributed to increase total body glucose uptake.…”

Section: Discussionmentioning

confidence: 99%

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Studies on the mass action effect of glucose in NIDDM and IDDM: evidence for glucose resistance

et al. 1997

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Tissue glucose uptake occurs via a facilitated transport system [1]. The major factors that regulate glucose uptake in vivo are the prevailing plasma glucose and insulin concentrations. Following glucose ingestion the plasma glucose concentration rises, insulin secretion is stimulated and the combination of hyperglycaemia and hyperinsulinaemia contributes to the increase in glucose utilization. Plasma glucose concentration influences glucose utilization by a mass Diabetologia (1997) Summary The ability of hyperglycaemia to enhance glucose uptake was evaluated in 9 non-insulin-dependent (NIDDM), 7 insulin-dependent (IDDM) diabetic subjects, and in 6 young and 9 older normal volunteers. Following overnight insulin-induced euglycaemia, a sequential three-step hyperglycaemic clamp (+ 2.8 + 5.6, and + 11.2 mmol/l above baseline) was performed with somatostatin plus replacing doses of basal insulin and glucagon, 3-3 H-glucose infusion and indirect calorimetry. In the control subjects as a whole, glucose disposal increased at each hyperglycaemic step (13.1 ± 0.6, 15.7 ± 0.7, and 26.3 ± 1.1 m mol/kg ⋅ min). In NIDDM (10.5 ± 0.2, 12.1 ± 1.0, and 17.5 ± 1.1 m mol/kg ⋅ min), and IDDM (11.2 ± 0.8, 12.9 ± 1.0, and 15.6 ± 1.1 m mol/kg ⋅ min) glucose disposal was lower during all three steps (p < 0.05-0.005). Hepatic glucose production declined proportionally to plasma glucose concentration to a similar extent in all four groups of patients. In control subjects, hyperglycaemia stimulated glucose oxidation (+ 4.4 ± 0.7 m mol/kg ⋅ min) only at + 11.2 mmol/l (p < 0.05), while non-oxidative glucose metabolism increased at each hyperglycaemic step (+ 3.1 ± 0.7; + 3.5 ± 0.9, and + 10.8 ± 1.7 m mol/kg ⋅ min; all p < 0.05). In diabetic patients, no increment in glucose oxidation was elicited even at the highest hyperglycaemic plateau (IDDM = + 0.5 ± 1.5; NIDDM = + 0.2 ± 0.6 m mol/kg ⋅ min) and non-oxidative glucose metabolism was hampered (IDDM = + 1.8 ± 1.5, + 3.1 ± 1.7, and + 4.3 ± 1.8; NIDDM = + 0.7 ± 0.6, 2.1 ± 0.9, and + 7.0 ± 0.8 m mol/kg ⋅ min; p < 0.05-0.005). Blood lactate concentration increased and plasma non-esterified fatty acid (NEFA) fell in control (p < 0.05) but not in diabetic subjects. The increments in blood lactate were correlated with the increase in non-oxidative glucose disposal and with the decrease in plasma NEFA. In conclusion: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. These results suggest that glucose resistance, that is the ability of glucose itself to promote glucose utilization, is impaired in both IDDM and NIDDM patients. [Diabetologia (1997) 40: 687-697] Keywords Hyperglycaemia, mass action effect, glucose-mediated glucose metabolism, glucose oxidation, non-oxidative glucose metabol...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Studies on the mass action effect of glucose in NIDDM and IDDM: evidence for glucose resistance

et al. 1997

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“…This effect has been shown in adult models (Siesjo, 1988), neonatal animal models (Anwar & Vannucci, 1988;Mujsce et al, 1989), and human infants (Pryds et al, 1988(Pryds et al, , 1990Pryds, 1991;Skov & Pryds, 1992). In human infants, a sharp increase in cerebral blood flow has been observed below a blood glucose of 30 mg/dL (Pryds et al, 1990).…”

Section: Initial Changesmentioning

confidence: 83%

“…There is dissociation between cerebral energy metabolism and brain functions during hypoglycemia. The changes in level of consciousness (from alert state to depressed state) and from normal EEG to slowing can occur with relatively little change in levels of ATP in various regions of brain (Siesjo, 1988;Vannucci et al, 1981;Vannucci & Vannucci, 2000;Volpe, 2008). This phenomenon can be attributed partially to metabolic changes happening during early periods of hypoglycemia.…”

Section: Initial Changesmentioning

confidence: 99%

An Update on Neonatal Hypoglycemia

Kumar¹,

Saini²

2011

Hypoglycemia - Causes and Occurrences

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“…It is well established that glucose passes across the blood brain barrier by carrier mediated transport (via GLUT 1 transporters) and unsaturable (diffusion) mechanisms [34]. Once in the ECF, the concentration of glucose seen by neurones and glia is, however, probably much lower than that of plasma.…”

Section: Brainmentioning

confidence: 99%