Hypoglycemia associated autonomic failure

Diedrich, Laura; Sandoval, Darleen A.; Davis, Stephen N.

doi:10.1007/s10286-002-0035-9

Cited by 36 publications

(21 citation statements)

References 63 publications

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“…In this context, hypoglycemia often occurs when insulin levels in excess of metabolic requirements are compounded by blunted neuroendocrine, autonomic nervous system (ANS) and metabolic counter-regulatory responses and associated symptoms. This phenomenon of blunted physiologic responses is referred to as hypoglycemia-associated autonomic failure (HAAF) and can occur in T1DM [11] and in insulin- and secretagogue-dependent T2DM populations [9,12–16]. When blood glucose goes unchecked and blunted symptoms go unnoticed (hypoglycemia unawareness) severe hypoglycemia ensues.…”

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confidence: 99%

Exercise-related hypoglycemia in diabetes mellitus

Younk

Mikeladze

Tate

et al. 2011

Expert Review of Endocrinology & Metabolism

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Current recommendations are that people with Type 1 and Type 2 diabetes mellitus exercise regularly. However, in cases in which insulin or insulin secretagogues are used to manage diabetes, patients have an increased risk of developing hypoglycemia, which is amplified during and after exercise. Repeated episodes of hypoglycemia blunt autonomic nervous system, neuroendocrine and metabolic defenses (counter-regulatory responses) against subsequent episodes of falling blood glucose levels during exercise. Likewise, antecedent exercise blunts counter-regulatory responses to subsequent hypoglycemia. This can lead to a vicious cycle, by which each episode of either exercise or hypoglycemia further blunts counter-regulatory responses. Although contemporary insulin therapies cannot fully mimic physiologic changes in insulin secretion, people with diabetes have several management options to avoid hypoglycemia during and after exercise, including regularly monitoring blood glucose, reducing basal and/or bolus insulin, and consuming supplemental carbohydrates. Keywordsexercise; hypoglycemia; hypoglycemia-associated autonomic failure; insulin; insulin secretagogues; physical activity; Type 1 diabetes mellitus; Type 2 diabetes mellitus Diabetes is a chronic disease state characterized by absolute or relative insulin deficiency and is a leading cause of death and disability in the USA. In 2008, the CDC reported that approximately 23.6 million people in the USA have diabetes and, of that population, 5.7 million cases are undiagnosed [1].Approximately 5-10% of individuals with diabetes have Type 1 diabetes mellitus (T1DM), an autoimmune disorder involving pancreatic β-cell destruction and consequent abolition of insulin secretion. Comprising the bulk (90-95%) of diabetes cases [1], Type 2 diabetes mellitus (T2DM) results from a combination of environmental and genetic factors, which lead to insufficient insulin secretion and insulin resistance.Diabetes can lead to an array of microvascular and macrovascular complications. It is the main cause of kidney failure, limb amputation and new-onset blindness in American adults

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confidence: 99%

Exercise-related hypoglycemia in diabetes mellitus

Younk

Mikeladze

Tate

et al. 2011

Expert Review of Endocrinology & Metabolism

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“…[7–9]). The systemic and glucose-sensing changes in response to RH, and mechanisms of hypoglycemia detection and counterregulation, are outside the scope of this mini-review which will focus solely on brain, and primarily cognitive, effects of RH.…”

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confidence: 99%

Mini-review: Impact of recurrent hypoglycemia on cognitive and brain function

McNay¹,

Cotero²

2010

Physiology & Behavior

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Recurrent hypoglycemia (RH), the most common side-effect of intensive insulin therapy for diabetes, is well established to diminish counterregulatory responses to further hypoglycemia. However, despite significant patient concern, the impact of RH on cognitive and neural function remains controversial. Here we review both the data from human studies and recent animal studies regarding the impact of RH on cognitive, metabolic, and neural processes. Overall, RH appears to causes brain adaptations which may enhance cognitive performance and fuel supply when euglycemic but which pose significant threats during future hypoglycemic episodes. Our brain runs on glucose: in contrast to cells elsewhere, which will generally take their fuel where they can find it, neurons and glia both rely on a constant supply of glucose from blood for their metabolic support (with some of that glucose being metabolised by astrocytes into lactate which is then exported for subsequent use by neurons). Unsurprisingly, acute interruption of this supply by systemic hypoglycemia produces marked cognitive impairment and leads eventually to coma and death. The consequences of acute hypoglycemia, including effects on cognitive and neural functions, are relatively wellunderstood. In addition and unsurprisingly, repeated severe hypoglycemia causes both significant neuronal death and cognitive impairment [1,2]. However, in recent years the impact on the brain and on cognitive functions of repeated, moderate interruptions of glucose supply, which cause little or no loss of neurons in hippocampus or cortex [3,4], has become of increasing interest. This interest is primarily the result of increased hypoglycemic incidence as a side-effect of advances in therapy for diabetes, but might also be of wider interest because of a potential relationship with the emerging practice of caloric restriction as an aid to long-term physical and mental health. The present review will examine data from both animal and human studies at a variety of levels of analysis. The primary conclusion drawn will be that the long-term consequences of moderate repeated hypoglycemia can be significant, but in general appear to be potentially beneficial at most times. There is, however, significant acerbation of the impact of further episodes of hypoglycemia on cognitive function, so that this risk should be recognised and borne in mind by those receiving or initiating protocols likely to produce such hypoglycemia.The most common cause of hypoglycemia in modern Western society is the use of exogenous insulin as a therapeutic agent for treatment of diabetes. Hypoglycemia has Mailing address: SS369,

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“…Exercise-induced hypoglycemia occurs up to 17 h after cessation of physical activity and can result from increased insulin sensitivity and glucose utilization. Furthermore, counterregulatory responses may be reduced by 50% during hypoglycemia following moderately intense exercise (16).…”

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confidence: 99%