The Impact of Insulin-Dependent Diabetes on  Ventilatory Control in the Mouse

Polotsky, Vsevolod Y.; Wilson, Jessica A.; Haines, Abby; Scharf, Matthew T.; Soutière, Shawn E.; Tankersley, Clarke G.; Smith, Philip L.; Schwartz, Alan R.; O’Donnell, Christopher P.

doi:10.1164/ajrccm.163.3.2007120

Cited by 57 publications

(36 citation statements)

References 29 publications

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“…Moreover, serum leptin was reduced in untreated DKA mice as observed in children with type-1 diabetes presenting with DKA (17). In contrast, leptin increases in untreated DKA in both human adults and in an adult mouse model of diabetes (24,34).…”

Section: Discussionmentioning

confidence: 88%

“…DKA was also observed in adult rats 48 h after injection with ALX (21), and in adult rabbits and dogs injected with STZ/ALX (22,23). The only mouse study to demonstrate ketosis involved STZ-treated adult mice fed a high-fat diet for 16 wk (24). We characterized a juvenile mouse model of DKA, as DKA-CE is almost exclusively a pediatric pathology (2,25).…”

Section: Discussionmentioning

confidence: 99%

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Combined Insulin and Bicarbonate Therapy Elicits Cerebral Edema in a Juvenile Mouse Model of Diabetic Ketoacidosis

Rose

Wang

et al. 2007

Pediatr Res

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Cerebral edema in diabetic ketoacidosis (DKA-CE) occurs primarily in children and can develop during DKA therapy. The treatment factors contributing to DKA-CE remain elusive. Our objectives were to characterize an age-appropriate DKA mouse model and to determine which DKA therapies contribute to DKA-CE. Juvenile mice were briefly fed a high-fat diet and injected with two pancreatic ␤-cell toxins: streptozocin and alloxan. Severe insulin and leptin deficiencies associated with hyperosmolar ketoacidosis rapidly developed, indicating DKA. DKA mice were treated with re-hydration Ϯ insulin and brain water content (BWC) measured as an indicator of DKA-CE. As expected, glucose and ␤-OH-butyrate corrected in DKA mice that received rehydration and insulin. BWC significantly increased above control levels only in DKA mice that received combined insulin and bicarbonate therapy, indicating the development of DKA-CE. Microscopically, DKA-CE brains had perineuronal and perivascular edema, with microvacuolation in the white matter tracts. These results indicate that insulin-deficient juvenile mice develop biochemical changes that are similar to those of DKA in children. Increased BWC was observed only in DKA mice that received combined insulin and bicarbonate therapy, suggesting that rapid systemic alkalinization in the presence of insulin may contribute to DKA-CE. (Pediatr Res 61: 301-306, 2007)

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Combined Insulin and Bicarbonate Therapy Elicits Cerebral Edema in a Juvenile Mouse Model of Diabetic Ketoacidosis

Rose

Wang

et al. 2007

Pediatr Res

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“…Weakness might result from nonenzymatic glycosylation (glycation) of muscle fibres ( fig. 4) [170,171]. Rarely, diaphragmatic weakness results from diabetic neuropathy of the phrenic nerves [172,173], which can occur despite the absence of peripheral neuropathy [173].…”

Section: Respiratory Musclesmentioning

confidence: 99%

Endocrinological derangements in COPD

Laghi

Adıgüzel²,

Tobin³

2009

European Respiratory Journal

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Chronic obstructive pulmonary disease (COPD) is no longer considered to affect only the lungs and airways but also the rest of the body. The systemic manifestations of COPD include a number of endocrine disorders, such as those involving the pituitary, the thyroid, the gonads, the adrenals and the pancreas.The mechanisms by which COPD alters endocrine function are incompletely understood but likely involve hypoxaemia, hypercapnia, systemic inflammation and glucocorticoid administration. Altered endocrine function can worsen the clinical manifestations of COPD through several mechanisms, including decreased protein anabolism, increased protein catabolism, nonenzymatic glycosylation and activation of the rennin-angiotensin-aldosterone system.Systemic effects of endocrine disorders include abnormalities in control of breathing, decreases in respiratory and limb-muscle mass and function, worsening of respiratory mechanics, impairment of cardiac function and disorders of fluid balance.Research on endocrine manifestations of COPD embraces techniques of molecular biology, integrative physiology and controlled clinical trials. A sound understanding of the various disorders of endocrine function associated with COPD is prudent for every physician who practices pulmonary medicine.

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“…Insulin-dependent diabetes mellitus can lead to an overall depression of ventilatory control mechanisms (19). Indeed, several studies have shown a strong association of obstructive sleep apnea syndrome (OSAS) with obesity, male gender (androidcentral obesity), post-menopausal women, hypertension and diabetes, factors associated with metabolic syndrome (20)(21)(22)(23)(24)(25).…”

Section: Implications Of Metabolic Impairments In Sleepmentioning

confidence: 99%

The reciprocal interaction between sleep and type 2 diabetes mellitus: facts and perspectives

Martins

Andersen

Tufik

2007

Braz J Med Biol Res

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Type 2 diabetes mellitus is a systemic disease characterized by intolerance to glucose and peripheral resistance to insulin. This endocrine disease affects fundamental mechanisms of the central nervous system and jeopardizes the balance of vital functions such as the cardiovascular and circadian rhythm. The increased prevalence of metabolic disorders in our society is aggravated by endemic voluntary postponement of bedtime and by the current sedentary lifestyle, leading to epidemic proportions of obese people. Diabetes and chronic loss of sleep share the fact that both affect millions and one is detrimental to the other. Indeed, sleep deficits have marked modulatory effects on glucose metabolism and insulin sensitivity and foster metabolic syndrome that culminates in sleep disorders like restless syndrome and sleep apnea, which in turn lead to poor sleep quality. We examine the hypothesis that these two worldwide emerging disorders are due to two interlinked cycles. In our paradigm, we establish an intimate relationship between diabetes and sleep disturbances and postulate possible mechanisms that provide support for this conjecture. In addition, we propose some perspectives about the development of the reciprocal interaction between predictor components of metabolic syndrome and sleep disturbances that lead to poor sleep quality. The ability to predict the development and identify or associate a given mode of sleep disturbance to diabetes would be a valuable asset in the assessment of both. Furthermore, major advances in care coupled with healthy lifestyles can ensure a higher quality of life for people with diabetes.

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The Impact of Insulin-Dependent Diabetes on Ventilatory Control in the Mouse

Cited by 57 publications

References 29 publications

Combined Insulin and Bicarbonate Therapy Elicits Cerebral Edema in a Juvenile Mouse Model of Diabetic Ketoacidosis

Combined Insulin and Bicarbonate Therapy Elicits Cerebral Edema in a Juvenile Mouse Model of Diabetic Ketoacidosis

Endocrinological derangements in COPD

The reciprocal interaction between sleep and type 2 diabetes mellitus: facts and perspectives

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