Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin‐dependent diabetes mellitus

Chiodera, P.; Volpi, R.; Capretti, L.; Speroni, G.; Necchi‐Ghiri, S.; Caffarri, G.; Colla, Rossana; Coiro, V.

doi:10.1046/j.1365-2265.1997.1470945.x

Cited by 34 publications

(16 citation statements)

References 43 publications

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“…Increased glucagon levels have also been shown after acute smoking in type 1 diabetic men though substantial changes in insulin sensitivity were not observed in these patients despite the rise in counter-regulatory hormones (107). Others have shown that smoking in patients with insulin-dependent diabetes not only elicits higher GH, AVP and cortisol responses than in normal subjects but also enhances the counter-regulatory responses to insulin-induced hypoglycaemia (108). These effects probably play a role in the pathogenesis of diabetic complications as increased cortisol and AVP cause an increase in blood pressure and thus their enhanced secretion in smokers might contribute to cardiovascular, cerebrovascular and renal diseases.…”

Section: Insulin Resistancementioning

confidence: 87%

Smoking and hormones in health and endocrine disorders

Kapoor¹,

Jones²

2005

eur j endocrinol

225

178

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Smoking has multiple effects on hormone secretion, some of which are associated with important clinical implications. These effects are mainly mediated by the pharmacological action of nicotine and also by toxins such as thiocyanate. Smoking affects pituitary, thyroid, adrenal, testicular and ovarian function, calcium metabolism and the action of insulin. The major salient clinical effects are the increased risk and severity of Graves' hyperthyroidism and opthalmopathy, osteoporosis and reduced fertility. Smoking also contributes to the development of insulin resistance and hence type 2 diabetes mellitus. An important concern is also the effect of smoking on the foetus and young children. Passive transfer of thiocyanate can cause disturbance of thyroid size and function. Furthermore, maternal smoking causes increased catecholamine production, which may contribute to under perfusion of the foetoplacental unit.European Journal of Endocrinology 152 491-499

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Section: Insulin Resistancementioning

confidence: 87%

Smoking and hormones in health and endocrine disorders

Kapoor¹,

Jones²

2005

eur j endocrinol

225

178

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“…The relation of smoking to severe hypoglycemia may be due to an effect of smoking on insulin clearance, leading to hyperinsulinemia, increasing the risk of postprandial hypoglycemia, and worsening metabolic control; such an effect was found in individuals with type 2 diabetes (13). In addition, smoking has been shown to increase the secretion of hormones (i.e., growth hormone, arginine vasopressin, and cortisol) that counteract insulin action, leading to an increased insulin requirement (14). Smokers have been found to require more insulin than nonsmokers to achieve the same level of glycemic control in some, but not all, studies (15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

Severe Hypoglycemia and Smoking in a Long-Term Type 1 Diabetic Population

et al. 2007

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OBJECTIVE -The purpose of this study was to evaluate the relationship of severe hypoglycemia and smoking in a population-based cohort of individuals with long-term type 1 diabetes.RESEARCH DESIGN AND METHODS -This was a cross-sectional analysis of the population-based cohort of the Wisconsin Epidemiologic Study of Diabetic Retinopathy. The analyses in this report were limited to 537 type 1 diabetic individuals with complete data who participated in the last examination phase (2000 -2001). Severe hypoglycemia was defined as having one or more episodes of loss of consciousness or overnight hospitalization attributable to hypoglycemia in a 1-year period before the examination.RESULTS -The prevalence of severe hypoglycemia in this population was 14.3%. In univariate analysis, current smokers had a greater chance of having severe hypoglycemia compared with never smokers (odds ratio 2.40 [95% CI 1.30 -4.40]). When we controlled for relevant confounders such as age, sex, A1C, waist-to-hip ratio, orthostatic hypotension, alcohol consumption, intensive insulin treatment, past history of severe hypoglycemia, and late complications of diabetes (nephropathy, neuropathy, and retinopathy), the association remained statistically significant, with current smoking presenting ϳ2.6 times greater odds of developing severe hypoglycemia.CONCLUSIONS -Current smokers with type 1 diabetes have higher odds of severe hypoglycemia episodes. Diabetes Care 30:1437-1441, 2007O ver the last few decades, new therapeutic agents have been introduced to improve glycemic control and reduce complications of type 1 diabetes. The Diabetes Control and Complications Trial showed the benefits of tight glycemic control, but it also showed that individuals receiving intensive insulin treatment had an increased risk of developing severe hypoglycemia. Thus, this complication remains a major challenge in treatment of diabetic patients (1-5). Age, diabetes duration, history of previous episodes of hypoglycemia, intensive insulin treatment, and lower levels of A1C have been described previously as factors associated with this complication (1-5). Smoking has been reported to be associated with hypoglycemia in previous clinical studies (6 -8), and it has been studied but not related to severe hypoglycemia in population-based studies. Smoking, through its effect on hormone regulation and insulin clearance, has been hypothesized to result in severe hypoglycemia (6 -8). The purpose of this study was to evaluate the relationship of severe hypoglycemia and smoking in a population-based study of individuals with long-term type 1 diabetes. (9). Participants were examined at baseline (n ϭ 996) and every 4 -6 years. The last examination phase (2000 -2001) was restricted to individuals (n ϭ 652) with type 1 diabetes. Detailed protocols used in this period were published elsewhere (10,11). Briefly, relevant evaluations included history of hypoglycemic reactions, neuropathy, nephropathy, cigarette smoking, and alcohol consumption; measurements of blood pressure in supine a...

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“…The rise in P VP after hypertonic saline infusion [8] or after cigarette smoking (a well-known stimulator of vasopressin release) and the fall in P VP observed after induction of hypoglycemia are greater in diabetics than in control subjects [14]. Along with vasopressin hypersecretion, the vasopressin content of the neurohypophysis is reduced in patients with uncontrolled type II DM [15], and the usual circadian rhythmicity in P VP observed in normal rats is lost in rats with uncontrolled type I DM [13].…”

Section: Vasopressin Elevation In Diabetes Mellitusmentioning

confidence: 99%

Vasopressin and Diabetes mellitus

Bankir¹,

Bardoux²,

Ahloulay³

2001

Nephron

100

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In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the developement of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.

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Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin‐dependent diabetes mellitus

Cited by 34 publications

References 43 publications

Smoking and hormones in health and endocrine disorders

Smoking and hormones in health and endocrine disorders

Severe Hypoglycemia and Smoking in a Long-Term Type 1 Diabetic Population

Vasopressin and Diabetes mellitus

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