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Purpose: The purposes of this study were to describe a newly developed algorithm that estimates the glucose supplement on a patient- and situation-specific basis and to test whether these amounts would be appropriate for maintaining blood glucose levels within the recommended range in exercising type 1 diabetic patients., Methods: The algorithm first estimates the overall amount of glucose oxidized during exercise on the basis of the patient's physical fitness, exercise intensity, and duration. The amount of supplemental CHO to be consumed before or during the effort represents a fraction of the burned quantity depending on the patient's usual therapy and insulin sensitivity and on the time of day the exercise is performed. The algorithm was tested in 27 patients by comparing the estimated amounts of supplemental CHO with the actual amounts required to complete 1-h constant-intensity walks. Each patient performed three trials, each of which started at different time intervals after insulin injection (81 walks were performed overall). Glycemia was tested every 15 min., Results: In 70.4% of the walks, independent of the time of day, the amount of CHO estimated by the algorithm would be adequate to allow the patients to complete the exercise with a glucose level within the selected thresholds (i.e., 3.9-10 mmol·L(-1))., Conclusions: The algorithm provided a satisfactory estimate of the CHO needed to complete the exercises. Although the performance of the algorithm still requires testing for different exercise intensities, durations, and modalities, the results indicate its potential usefulness as a tool for preventing immediate exercise-induced glycemic imbalances (i.e., during exercise) in type 1 diabetic patients, in particular for spontaneous physical activities not planned in advance, thus allowing all insulin-dependent patients to safely enjoy the benefits of exercise.

Purpose: The purpose of this study was to evaluate the effects of restless legs syndrome (RLS) on quality of life (QoL), anxiety, and depression in people with type 2 diabetes., Methods: One hundred twenty-four patients with type 2 diabetes were enrolled in this study. RLS was diagnosed by a neurologist masked on psychological evaluation. Data on severity, frequency, and duration of the sleep disorder were collected. The Italian version of the SF-36 was used to assess QoL. Psychological status was investigated by a neuropsychologist masked on RLS diagnosis. Patients with a diagnosis of generalized anxiety disorder (GAD) and major depressive disorder (MDD) were considered affected by anxiety and depression, respectively. A modified version of the Hamilton Anxiety and Depression Rating Scales (HARS and HDRS) was also administered., Results: RLS was an independent predictor for several mental domains of the SF-36 and for the mental component summary. Multivariate analysis showed that RLS was an independent predictor of anxiety and depression. RLS severity correlated with HARS and HDRS scores, whereas frequency per week of RLS had a significant correlation only with HARS score., Conclusions: Among individuals with diabetes, RLS can impair mental health, increasing the risk for anxiety and depression. Since RLS consequences on nocturnal rest and psychological status may impair glycemic control in this population, diabetologists and diabetes educators should investigate for the presence of RLS in their patients and treat them.

Background and Aims: To compare switching from NPH insulin (NPH) to insulin glargine (glargine) with continuing NPH for changes in fasting blood glucose (FBG) in patients with Type 1 diabetes on basal-bolus therapy with insulin lispro as bolus insulin. Secondary objectives included self-monitoring blood glucose, mean daily blood glucose (MDBG) and mean amplitude glucose excursion (MAGE) values alongside changes in HbA(1c) and safety profiles., Methods and Results: This was a 30-week, parallel, open-label, multicentre study. Seven-point profiles were used to calculate MDBG and MAGE. Hypoglycaemia and adverse events were recorded by participants. FBG improved significantly with both glargine (baseline-endpoint change: -28.0 mg/dL; 95% CI: -37.3, -18.7 mg/dL; p<0.001) and NPH (-9.8 mg/dL; 95% CI: -19.1, -0.5 mg/dL; p=0.0374). The improvement was significantly greater with glargine than NPH (mean difference: -18.2 mg/dL; 95% CI: -31.3, -5.2 mg/dL; p=0.0064). MDBG (-10.1 mg/dL; 95% CI: -18.1, -2.1 mg/dL; p=0.0126) and MAGE (-20.0 mg/dL; 95% CI: -34.5, -5.9 mg/dL; p=0.0056) decreased significantly with glargine, but not NPH although endpoint values were no different with the two insulins. Baseline to endpoint change in HbA(1c) was similar (-0.56 vs -0.56%) with no differences at endpoint. Overall hypoglycaemia was no different, but glargine reduced nocturnal hypoglycaemia ("serious episodes" with BG < 42 mg/dl, p=0.006) whereas NPH did not (p=0.123), although endpoint values were no different., Conclusion: Switching from NPH to glargine is well tolerated and results into lower FBG, and lower glucose variability while reducing nocturnal hypoglycaemia. These data provide a rationale for more aggressive titration to target with glargine in Type 1 diabetes.

Study Objective: To look for an association between restless legs syndrome (RLS) and type 2 diabetes in a case-control study; to analyze the characteristics of RLS in diabetic patients; and to identify possible risk factors for the development of RLS in diabetic patients., Design: A case-control study., Setting: Diabetic outpatient clinic of a major university hospital., Participants: One hundred twenty-four consecutive outpatients with diabetes and 87 consecutive controls with a previous diagnosis of other endocrine disease., Interventions: RLS was diagnosed using the criteria of the International RLS Study Group, and severity of RLS was assessed using the International RLS Study Group Rating Scale. Characteristics of RLS and several laboratory parameters were investigated in diabetic patients and controls affected by the sleep disorder. A clinical diagnosis of polyneuropathy was assessed to evaluate its role as a risk factor for RLS in diabetic patients., Measurement and Results: RLS was diagnosed in 22 diabetic patients (17.7%) and in only 5 controls (5.5%), 3 of whom had pituitary and 2 had adrenal gland disorders, and RLS was independently associated with type 2 diabetes (P < 0.04). Even if a clinical diagnosis of polyneuropathy was made in only 27% of diabetic patients affected by RLS, after multivariate logistic regression, the presence of polyneuropathy was the only variable associated with RLS in diabetics (odds ratio, 7.88; 95% confidence interval, 1.34-46.28; P < 0.02). RLS in diabetics showed a frequency of positive family history lower than that known for primary RLS, showed a late age of onset, and manifested itself after the diagnosis of diabetes was made., Conclusions: This is the first controlled study confirming a significant association between RLS and type 2 diabetes. In diabetic patients, polyneuropathy represents the main risk factor for RLS. However, polyneuropathy only partially explains the increased prevalence of RLS in type 2 diabetics. Clinical characteristics of RLS in diabetic patients are those of a secondary form.

The lack in control of insulin release combined with an inadequate carbohydrate (CHO) ingestion accounts for the occurrence of frequent metabolic unbalances during exercise in type 1 diabetic patients. The aim of the study was to quantify, in these patients, the CHO requirement to prevent hypoglycemia during moderate exercise performed at different time intervals after morning subcutaneous insulin injection. Twelve type 1 diabetic patients and 12 well-matched healthy subjects cycled 4 times for 1 hour at a constant workload. The rate of glucose oxidation was calculated continuously by indirect calorimetry throughout the exercise, while blood parameters were assessed periodically and orally given CHO were checked. CHO needed by the patients to prevent hypoglycemia decreased as the time elapsed from insulin administration increased, amounting to 0.63 +/- 0.30, 0.44 +/- 0.32, 0.28 +/- 0.24, and 0.14 +/- 0.18 g/kg after 1, 2.5, 4, and 5.5 hours, respectively. Total glucose requirement during moderate exercise (sum of alimentary and extracellular source) was correlated (r = 0.739, P <.001) to plasma insulin concentration, but not with fitness level. Time elapsed from last insulin dose is not a factor influencing the risk of hypoglycemia during exercise when a proportional, appropriate amount of CHO is ingested.

The aim of this study was to compare glucose measurements between fingertip and forearm using the blood glucose (BG) monitoring system One Touch Ultra (LifeScan), an electrochemical sensor that requires only a very small drop of blood (1 microL). Patients with type 1 or type 2 diabetes were identified in five outpatient diabetes clinics. Participants were requested to use the One Touch Ultra at home for 1 week for the measurement of BG levels from both sites. Patients filled in a questionnaire about their experience with testing blood samples from fingertip and forearm. The agreement between the measurements from the two sites was assessed using linear regression analysis, mean absolute relative error (MARE), the Bland-Altman method, and Error Grid Analysis (EGA). Overall, 112 patients were recruited, of whom 58% had type 1 diabetes. Linear regression analysis showed an intercept of 17.7, statistically different from 0 (p<0.0001). The slope was 0.956, and the Pearson correlation coefficient was 0.95. A MARE of 12.1% (SD=11.8%) was obtained, with a greater deviation of the forearm values from the fingertip ones in the hypoglycemic range (MARE=22.3%; SD=21.7%). The Bland-Altman bias plot showed a mean bias of 10.2 mg/dL (SD=23.1), with no correlation between mean difference and average BG levels (r=0.02). The EGA showed that 89.2% of the values fell in zone A, 10.4% in zone B, and 0.4% in zone C. The vast majority of patients (71%) declared that the collection of blood from the forearm caused no pain or less pain than the traditional site. Only 17% of the patients declared that it was impossible to obtain any blood from the forearm, while 63% reported with satisfaction that the quantity requested was small. At the end of the study period, 32% of the participants indicated the forearm as the preferred test site. Alternative site testing on the arm, with a BG meter that requires only a very small drop of blood, is feasible and reliable under routine clinical conditions. When testing with the express purpose of detecting hypoglycemia, the finger still remains the recommended test site.

Nicotinamide was shown to prevent damage and to stimulate B cell regeneration in experimental diabetes but in humans results are still controversial. To ascertain if long term nicotinamide treatment can induce and/or prolong remission of the disease, 21 type 1 (insulin-dependent) recently diagnosed subjects entered a controlled study and randomly divided in two groups comparable for age, genetic and immunologic patterns: group 1 (11 subjects) received insulin and nicotinamide (3 g/day for 1 year) and group 2 (10 subjects) insulin alone. Bimonthly insulin requirement and HbA1c, and every 6 months C-peptide response to glucagon were registered for 2 years. No significant difference was observed between the two groups in the monitored parameters, including rates of clinical remission, along this time period. In conclusion nicotinamide, when employed after the clinical onset of the disease, has no additional effect on natural history of newly diagnosed type 1 diabetes mellitus, besides results obtained by insulin alone.

Atherosclerotic manifestations are more common and precocious in diabetics than in the general population. Due to the increased cardiovascular risk, a primary or secondary (to diabetes mellitus) lipoprotein disorder in diabetics has to be carefully considered. 27 diabetics (15 NIDDM and 12 IDDM) with dyslipidemia (14 type IV, 8 type IIa and 5 type IIb) were divided in 3 groups and treated with 3 different hypolipemic drugs (Group A: pantethine 600 mg/day; Group B: acipimox 500 mg/day; Group C: bezafibrate 600 mg/day) to test their efficacy and acceptancy. Body weight, Hb A1-c, serum lipoproteins have been measured before and during the 6 months treatment. A significant variation of lipidemic pattern was observed in Group C: a decrease of cholesterol (-20%), triglycerides (-40%), LDL (-24.4%) and apo B (-26.8%) with an increase of HDL (+23.6%). Pantethine and acipimox were more effective on triglycerides (-37.7% and -23.3% respectively). Cardiovascular risk (CT tot/CT HDL) was significantly reduced with acipimox and normalized with bezafibrate.

Physical exercise is a well known provocative test for early renal abnormalities detection in diabetes mellitus. Aim of our study was to evaluate the effect of daily activity and physical exercise on albumin excretion rate (AER) in 2 groups of albustix negative type I diabetics (IDDM). In group I of 76 patients aged 7-58 years, AER measured in 24 h urine (14.1 +/- 1.7 micrograms/min) and overnight urine (11.1 +/- 1.7 micrograms/min) was similar. A significant correlation was found between AER values obtained from the two urine collection procedures (r = 0.55; p less than 0.001). In group 2 of 37 patients aged 7-48 years and in 25 matched controls, the effect of physical exercise on AER was evaluated comparing overnight urine and post-exercise urine collection. AER increased significantly in IDDM after exercise. In conclusion our results show that 1) AER is not affected by daily activity; 2) physical exercise is a usefull provocative test to detect early renal abnormalities.

To examine whether abnormal pancreatic alpha-cell function found in human diabetes mellitus may represent a selective insensitivity to glucose, plasma glucagon responses to hyperglycemia and elevation of plasma free fatty acid levels (both known suppressors of glucagon secretion) were compared in juvenile-onset, insulin-requiring diabetic subjects, and in normal nondiabetic subjects. In the latter, both elevation of plasma free fatty acid levels induced by heparin administration of hyperglycemia produced by intravenous infusion of glucose resulted in a comparable 30--40% suppression of circulating glucagon levels (P less than 0.01). In the diabetic subjects, glucagon suppression by hyperglycemia (less than 20%) was less than that occurring in normal subjects (P less than 0.01), even when accompanied by infusion of supraphysiologic amounts of insulin. However, suppression of glucagon levels by elevation of plasma free fatty acids in the diabetic group was similar to that found in normal subjects and of comparable magnitude to that due to hyperglycemia in the normal subjects. These results thus demonstrate a selective impairment of the diabetic alpha-cell response to glucose and provide further evidence for the presence of an abnormal alpha-cell glucoreceptor in human diabetes mellitus.

The present investigation was undertaken to ascertain whether alterations in plasma free fatty acids (FFA) affect pancreatic glucagon secretion in man since FFA have been reported to influence pancreatic alpha cell function in other species. Elevation of plasma FFA from a mean (+/-SE) basal level of 0.478+/-0.036 mM to 0.712+/-0.055 mM after heparin administration caused plasma glucagon levels to fall approximately 50%, from a basal value of 122+/-15 pg/ml to 59+/-14 pg/ml (P < 0.001). Lowering of plasma FFA from a basal level of 0.520+/-0.046 mM to 0.252+/-0.041 mM after nicotinic acid administration raised plasma glucagon from a basal level of 113+/-18 pg/ml to 168+/-12 pg/ml (P < 0.005). Infusion of glucose elevated plasma glucose levels to the same degree that heparin raised plasma FFA levels. This resulted in suppression of plasma glucagon despite the fact that plasma FFA levels also were suppressed. Glucagon responses to arginine were diminished after elevation of plasma FFA (P < 0.01) and during infusion of glucose (P < 0.01). Diminution of plasma FFA by nicotinic acid did not augment glucagon responses to arginine. These results thus demonstrate that rather small alterations in plasma FFA within the physiologic range have a significant effect on glucagon secretion in man. Although the effects of glucose appear to predominate over those of FFA, alterations in plasma FFA may nevertheless exert an important physiologic influence over human pancreatic alpha cell function, especially in the postabsorptive state.

In order to characterize the influence of the adrenergic system on pancreatic glucagon secretion in man, changes in basal glucagon secretion during infusions of pure alpha and beta adrenergic agonists and their specific antagonists were studied. During infusion of isoproterenol (3 mug/min), a beta adrenergic agonist, plasma glucagon rose from a mean (+/-SE) basal level of 104+/-10 to 171+/-15 pg/ml, P < 0.0002. Concomitant infusion of propranolol (80 mug/min), a beta adrenergic antagonist, prevented the effects of isoproterenol, although propranolol itself had no effect on basal glucagon secretion. During infusion of methoxamine (0.5 mg/min), an alpha adrenergic agonist, plasma glucagon declined from a mean basal level of 122+/-15 to 75+/-17 pg/ml, P < 0.001. Infusion of phentolamine (0.5 mg/min), an alpha adrenergic antagonist, caused a rise in plasma glucagon from a mean basal level of 118+/-16 to 175+/-21 pg/ml, P < 0.0001. Concomitant infusion of methoxamine with phentolamine caused a reversal of the effects of phentolamine. The present studies thus confirm that catecholamines affect glucagon secretion in man and demonstrate that the pancreatic alpha cell possesses both alpha and beta adrenergic receptors. Beta adrenergic stimulation augments basal glucagon secretion, while alpha adrenergic stimulation diminishes basal glucagon secretion. Furthermore, since infusion of phentolamine, an alpha adrenergic antagonist, resulted in an elevation of basal plasma glucagon levels, there appears to be an inhibitory alpha adrenergic tone governing basal glucagon secretion. The above findings suggest that catecholamines may influence glucose homeostasis in man through their effects on both pancreatic alpha and beta cell function.

A peculiar involvement of the interphalangeal joints of both hands with palmar flexion of the fingers has been observed in 11 insulin-treated, nonrheumatoid, juvenile diabetics. The onset of diabetes occurred between 1 and 12 years of age. Painless deformities of the fingers with progressive stiffness and impaired extension started 4 to 10 years later. One patient complained of articular pain and swelling. X-ray and circulatory changes were absent or minimal. Prepubertal patients showed delayed puberty and stunted growth, adult patients had normal sexual development. Rheumatic or rheumatoid signs were absent. Electromyography showed minor abnormalities of the motor units, normal or subnormal motor nerve conduction velocity, increased median nerve terminal latency, in the absence of muscular atrophy or thickening of palmar tendons. Vibratory sensitivity was impaired in 1 subject. Juvenile cheiroarthropathy is associated with: a) early onset and poor control of diabetes; b) stunted growth; c) hepatomegaly; d) delayed puberty; e) long standing administration of insulin. The articular changes are distinct from previously known forms of "diabetic hand", such as atrophic neuropathy, osteoarthropathy, Dupuytren's contracture, carpal tunnel syndrome.

A family with primary isolated hypoparathyroidism transmitted by an autosomal dominant gene was documented; the proband was a 38-year-old woman with a history of weakness and carpopedal spasm. The family study revealed that 6 out of 13 members belonging to 3 generations were affected by hypoparathyroidism without any evidence of an autoimmune disease. Vertical male-to-male, female-to-female and female-to-male transmission were demonstrated. Having excluded the recessive form of familial hypoparathyroidism, pseudohypoparathyroidism, primary familial hypomagnesemia and any immunological disorder, the autosomal dominant inheritance seems to be the most important etiology of idiopathic hypoparathyroidism.

Despite excessive glucagon responses to infusion of arginine, plasma glucagon did not rise in six juvenile-type diabetics during severe insulin-induced hypoglycemia, whereas glucagon in the controls rose significantly. Thus in diabetics pancreatic alpha cells are insensitive to glucose even in the presence of large amounts of circulating insulin. An intrinsic defect common to both alpha and beta pancreatic cells-failure to recognize (or respond to) plasma glucose fluctuations-may be operative in juvenile diabetes.