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Enamel hypoplasia in a litter of rats with alloxan-induced diabetes mellitus.

Enamel hypoplasia is an important clinical problem commonly seen in children born to diabetic women. We aimed to characterize the enamel hypoplasia in Wistar rats born to alloxan-induced diabetes mellitus rats. Groups consisted of pregnant rats supplemented (ISDR) or not (NISDR) with insulin and controls, in which sterile saline solution was administered instead of alloxan or insulin. The mandibular incisors of one-month-old rats born to these mothers were analyzed. Whitish defective enamel was found macroscopically in both experimental groups (ISDR = 37.5%, NISDR = 33.3%) but not in the control group. Mild to severe enamel hypoplasia was observed by scanning electron microscopy (ISDR = 93.8%; NISDR = 100%, control = 4.2%). The severity of hypoplasia correlated positively with the maternal level of blood glucose. In conclusion, the intensity of enamel hypoplasia in the teeth of the litter born to alloxan-induced diabetic rats was variable and was dependent on the glycemic level of the pregnant rat.

Alloxan↗

Abnormalities of glucose metabolism induced by liver cirrhosis and glycosylated hemoglobin levels in chronic liver disease.

UNLABELLED: The prevalence of impaired glucose tolerance (IGT) and diabetes mellitus (DM) such as defined by National Diabetes Data Group criteria, and glycosylated hemoglobin levels were assessed in a series of consecutive patients who had chronic active hepatitis (CAH) or cirrhosis in the absence of any known diabetogenic risk factors and who had normal fasting glycemic levels. Based on oral glucose tolerance test, the prevalence of IGT (15%) and DM (27%) in cirrhosis was significantly higher (p less than 0.005) than that observed in CAH (0%) and controls (0%). In contrast, HbA1 levels were not statistically different in cirrhotic patients (with normal or altered glucose tolerance) as compared with CAH and control subjects. IN CONCLUSION: (a) HbA1 is an unsatisfactory test in the diagnosis of altered glucose tolerance in patients with cirrhosis, and (b) Cirrhosis (but not CAH) represents itself a risk factor for the development of glucose metabolism alterations. Therefore, routine oral glucose tolerance testing is warranted in these patients.

Adult↗

Exogenous insulin administration and cardiovascular risk in non-insulin-dependent and insulin-dependent diabetes mellitus.

PURPOSE: It is currently unknown whether intensive insulin treatment of diabetes decreases the risk for cardiovascular complications by lowering glucose levels or increases the risk by postulated direct atherogenic effects. This article reviews published data from two long-term, randomized clinical trials that compared cardiovascular outcomes associated with different exogenous insulin treatment regimens. STUDY SELECTION AND DATA SOURCES: The University Group Diabetes Program (UGDP) and the Diabetes Control and Complications Trial (DCCT) were selected as the only available randomized intervention trials with long-term follow-up results. Data reviewed were from the major publications of these two trials. RESULTS: The UGDP compared the effects of a fixed-dose standard insulin regimen, a variable-dose insulin regimen, and a diet plus oral placebo regimen in over 600 patients with non-insulin-dependent diabetes mellitus (NIDDM) who were followed for up to 13 years (1962 to 1975). Plasma glucose levels were 1.7 to 2.2 mmol/L lower in the variable-dose insulin regimen group than in the other two treatment groups. No significant differences were found in the final prevalence or the cumulative incidence of total deaths, cardiovascular disease deaths, or myocardial infarctions among the three treatment groups, even when outcomes were adjusted for pertinent baseline cardiovascular risk factors. There was a slight suggestion only from post hoc analysis that patients in both insulin treatment groups, who were defined as having good glucose control, had fewer cardiovascular events than those with fair or poor control. The DCCT compared intensive insulin treatment with conventional insulin treatment (the mean hemoglobin A1c [HbA1c] level was 7.2% and 9.0%, respectively) in over 1400 patients with insulin-dependent diabetes (IDDM) followed for up to 10 years (1983 to 1993). Three major cardiovascular events occurred in the intensive treatment group as compared with 14 in the conventional treatment group (P > 0.05), and low-density lipoprotein cholesterol and triglyceride levels were substantially lower in the intensive treatment group. However, body mass index increased substantially more with intensive than with conventional therapy. CONCLUSIONS: The UGDP trial was flawed by inadequate power, insufficient separation of glycemic levels, and ignorance of smoking history as a possible confounder. In the DCCT, the number of cardiovascular events was few because the patients were young and had a relatively short duration of diabetes at baseline. In addition, total daily insulin doses were similar in the two DCCT treatment groups. For these reasons, neither trial provides a definitive answer to the question about the effects of intensive insulin therapy. A better designed clinical trial is needed to determine whether insulin treatment has beneficial or adverse effects, or even offsetting beneficial and adverse effects, on the risk for cardiovascular disease in NIDDM and IDDM.

Blood Glucose↗

Similar reduction of first- and second-phase B-cell responses at three different glucose levels in type II diabetes and the effect of gliclazide therapy.

To characterize the abnormal B-cell response to glucose in type II diabetes, five diet-treated diabetic and six weight-matched non-diabetic subjects were studied using the hyperglycemic clamp technique on three separate days at glycemic levels of 7.5, 10 and 15 mmol/L for 150 minutes with assessment of plasma insulin and C-peptide responses. To reduce possible secondary effects of hyperglycemia, diabetic subjects on a weight-maintaining diet were chosen who had only a slight elevation of the fasting plasma glucose, mean 6.0 mmol/L. They had a normal time-course of both first- and second-phase responses, but both were impaired at each glucose clamp concentration. The first-phase and second-phase C-peptide responses of the diabetic subjects were similarly reduced to mean 49% and 59% of normal, respectively, and the first- and second-phase insulin responses were also reduced to mean 39% and 44% of normal, respectively. The ratio of second- to first-phase plasma C-peptide responses were similar in the diabetic and normal subjects, median 1.6 and 1.5, respectively, as were the same ratios for the insulin responses, 1.4 and 1.1, respectively. The previously described selective reduction of the first-phase response in type II diabetes may be partly a function of the bolus intravenous glucose tests used, in which impaired glucose tolerance in the diabetics gave a greater glycemic stimulus to the second phase than in normal subjects, and partly secondary to long-term hyperglycemia. The diabetic subjects were re-studied after treatment with a sulphonylurea, gliclazide, with a normal fasting plasma glucose, mean 5.1 mmol/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Oxidative stress: changes in pregnancy and with gestational diabetes mellitus.

Pregnancy is susceptible to oxidative stress and antioxidant defenses can be altered in response to elevated levels of oxidative stress. Limited data in gestational diabetes mellitus (GDM) suggest that products of lipid peroxidation may be increased and antioxidant enzyme activities decreased, although the results have been inconsistent. As in type 2 diabetes mellitus (T2DM), glycemic levels in patients with GDM correlate with concentrations of lipid peroxides. The effects of supplementation with antioxidants or antioxidant-rich food in T2DM are controversial. Whether or not increased antioxidant intake can reduce the complications of GDM in both mother and fetus has not been explored.

Antioxidants↗

Regulation of glucagon secretion by glucose transporter type 2 (glut2) and astrocyte-dependent glucose sensors.

Ripglut1;glut2-/- mice have no endogenous glucose transporter type 2 (glut2) gene expression but rescue glucose-regulated insulin secretion. Control of glucagon plasma levels is, however, abnormal, with fed hyperglucagonemia and insensitivity to physiological hypo- or hyperglycemia, indicating that GLUT2-dependent sensors control glucagon secretion. Here, we evaluated whether these sensors were located centrally and whether GLUT2 was expressed in glial cells or in neurons. We showed that ripglut1;glut2-/- mice failed to increase plasma glucagon levels following glucoprivation induced either by i.p. or intracerebroventricular 2-deoxy-D-glucose injections. This was accompanied by failure of 2-deoxy-D-glucose injections to activate c-Fos-like immunoreactivity in the nucleus of the tractus solitarius and the dorsal motor nucleus of the vagus. When glut2 was expressed by transgenesis in glial cells but not in neurons of ripglut1;glut2-/- mice, stimulated glucagon secretion was restored as was c-Fos-like immunoreactive labeling in the brainstem. When ripglut1;glut2-/- mice were backcrossed into the C57BL/6 genetic background, fed plasma glucagon levels were also elevated due to abnormal autonomic input to the alpha cells; glucagon secretion was, however, stimulated by hypoglycemic stimuli to levels similar to those in control mice. These studies identify the existence of central glucose sensors requiring glut2 expression in glial cells and therefore functional coupling between glial cells and neurons. These sensors may be activated at different glycemic levels depending on the genetic background.

Animals↗

Effect of quality improvement on racial disparities in diabetes care.

BACKGROUND: Racial disparities in care are well documented; information regarding solutions is limited. We evaluated whether generic quality improvement efforts were associated with changes in racial disparities in diabetes care. METHODS: Using insurance claims and electronic medical record data, we identified 5101 whites and 1987 blacks with diabetes mellitus receiving care within a multispecialty group practice from 1997 to 2001. We assessed rates of annual low-density lipoprotein cholesterol level testing, low-density lipoprotein cholesterol level control (<130 mg/dL [<3.37 mmol/L]), statin therapy, annual glycosylated hemoglobin level testing, glycosylated hemoglobin level control (<7.0%), and annual dilated eye examinations. We used logistic regression models with generalized estimating equations to adjust for race, year, race x year interactions, age, and sex. RESULTS: Rates of annual low-density lipoprotein cholesterol level testing increased from 39% to 64%, while the white-black disparity decreased from 14% to 4%; rates of low-density lipoprotein cholesterol level control increased from 15% to 43%, while the white-black disparity decreased from 9% to 6% (P<.001 for both race x year interactions). Statin therapy rates increased from 20% to 37%; however, black patients remained less likely than white patients to receive therapy. The 1997 rates of annual glycosylated hemoglobin level testing (76%) and annual eye examinations (74%) were high, and there was no white-black disparity over time. Rates of glycosylated hemoglobin level control remained low (31%), and the white-black disparity remained constant at 10%. CONCLUSIONS: Racial disparities were diminished in some aspects of diabetes care following variably successful quality improvement, but differences in the use of statins and glycemic level control persisted. Reducing disparities may require a focus on minority health.

Black People↗

Dose-dependent effect of octreotide on insulin secretion after OGTT in obesity.

OBJECTIVE: The present study aimed at evaluating the acute effect of increasing doses of octreotide (OCT), a long-acting somatostatin analogue, on glucose tolerance and insulin secretion. METHODS: A standard and two other oral glucose tolerance tests 30 min after subcutaneous administration of OCT were performed in randomized order in each subject. Obese subjects received 10, 25, or 50 microg of OCT; control subjects received only 10 and 25 microg. Fifteen obese and 10 control subjects were studied; all of them had a normal glucose tolerance. Plasma glucose and insulin levels were measured at times -30, 0, 30, 60, 90, 120, 150, and 180 min after the glucose tolerance test. RESULTS: The results demonstrated that, following OCT administration, both control and obese subjects developed a reduced glucose tolerance, a delayed glycemic peak, and an increase of late plasma glucose values. Fasting as well as stimulated insulin secretions were higher in obese subjects as compared with controls, and insulin secretion was inhibited in a dose-dependent manner by OCT. CONCLUSIONS: These data indicate that the action of OCT might be due to at least two different cooperative mechanisms: (1) a delayed glucose absorption, as suggested by the delay of glycemic peak, and (2) a direct or vagal-mediated effect on beta-cells, as suggested by the reduction of the area under the curve values in spite of the elevated late glycemic levels. It is noteworthy that doses of OCT as low as 10 and 25 microg are sufficient to inhibit insulin secretion both in normal and obese subjects.

Adult↗

Pituitary cotransplantation significantly improves the performance, insulin content, and vascularization of renal subcapsular islet grafts.

Because the pituitary contains hormones with beta-cell trophic activity, we evaluated whether cotransplantation of pituitary tissue with pancreatic islets might be beneficial for islet graft function and survival. Streptozotocin diabetic nude mice were transplanted under the kidney capsule with 150 handpicked islets alone or mixed with two diced pituitaries and were then followed for 4 weeks. Mice transplanted with mixed islet/pituitary grafts had higher levels of circulating prolactin (PRL) than mice transplanted with islets only, while serum cortisol, growth hormone, and follicle-stimulating hormone were similar in the two groups. After transplantation, recipients of mixed islet/pituitary grafts showed a more pronounced decrease in glycemic levels and higher systemic insulin levels than mice transplanted only with islets. Mixed islet/pituitary grafts were macroscopically characterized by an excellent vascularization and were biochemically characterized by higher insulin and PRL content than pure islet grafts. Histologically, posttransplantation remodeling originated a hybrid organ in which healthy, well-vascularized islets were adjacent to pituitary cell clusters. Transplantations performed to address the specific effect of the anterior versus the intermediate pituitary lobes indicated the former as responsible for the improved function of cotransplanted islets. Mixed islet/pituitary grafts composed of anterior lobes were also the best vascularized and were histologically characterized by the presence of many folliculo-stellate cells. In conclusion, we obtained evidence that pituitary cotransplantation significantly improves the function, insulin content, and vascularization of suboptimal islet grafts. Evidence suggesting that ectopically produced PRL and/or locally released angiogenic peptides might play a causal role is provided.

Animals↗

How to minimize missing those subjects with high 2HR plasma glucose but 'normal' fasting plasma glucose levels?

Among the subjects with 'normal' fasting plasma glucose (PG) levels (< 7.0 mmol/L), some of them are actually suffering from impaired glucose tolerance and diabetes, which can only be diagnosed by 2hr PG levels. We aim to find out a proper clinical approach in order to minimize missing those subjects with high 2hr PG but 'normal' fasting PG levels. We analyzed data collected from a previously published population-based prevalence survey for glucose intolerance in 1486 Hong Kong Chinese subjects who had no past history of diabetes. Of the 1468 subjects, there were 138 subjects (9.4%) having "missed glucose intolerance". Compared to the diabetic subjects (fasting plasma glucose > or = 7.0 mmol/L) after adjustment for age, the subjects with missed glucose intolerance had similar characteristics except lower glycemic level. Compared to the normal subjects (fasting plasma glucose < 7.0 mmol/L) after adjustment for age, subjects with missed glucose intolerance had more obesity (both general and central), more hypertension, worse glycemic status and lipid profile in both men and women. There were 38 subjects (2.6%) having impaired fasting glucose. Of these 38 subjects, 24 (63.2%) had missed glucose intolerance. The detection of missed glucose intolerance increased from 9.7% of overall male subjects to 23.1% in men with hypertension to 52.9% in men with both hypertension and family history of diabetes. Similarly, the detection of missed glucose intolerance increased from 9.0% of overall female subjects to 25.7% in women with obesity to 45.2% in women with both obesity and hypertension. If only fasting plasma glucose is performed, 4% of subjects will be diagnosed to have diabetes or impaired fasting glucose while up to 10% of subjects having impaired glucose tolerance or diabetes will be missed in Hong Kong Chinese. The latter 2 groups of subjects have similar cardiovascular risk factors to those with fasting PG > or = 7.0 mmol/L. We recommend that for those with a family history of diabetes, hypertension or obesity, an oral glucose tolerance test instead of fasting plasma glucose should be used in the first place for the diagnosis of glucose intolerance. For those with impaired fasting glucose, a routine follow-up oral glucose tolerance test should also be performed. This clinical approach may improve the detection of those subjects with glucose intolerance, who will be otherwise missed by using fasting plasma glucose alone.

Adult↗

Current treatment approaches to type 2 diabetes mellitus: successes and shortcomings.

Diabetes mellitus affects approximately 17 million adults in the United States and has profound implications in terms of long-term microvascular and macrovascular complications and their associated costs. In type 2 diabetes, insulin resistance and a relative beta-cell defect are the underlying pathologic problems leading to hyperglycemia. Notably, insulin resistance is also associated with obesity, dyslipidemia, and hypertension. Diabetes can be defined as a disease of accelerated cardiovascular deterioration associated with elevated blood glucose levels. Glycemic control has been shown to reduce the long-term complications associated with diabetes. Although medical nutrition therapy and appropriately prescribed increased physical activity are important components of a diabetes management plan, most patients need medication to lower glucose to near-normal levels. Therapeutic options for treating hyperglycemia include sulfonylureas and other insulin secretagogues, biguanides, alpha-glucosidase inhibitors, thiazolidinediones, and insulin. An antidiabetic agent that improves insulin sensitivity is an excellent choice for early treatment of type 2 diabetes because it may delay or prevent complications associated with this disease. Because of the progressive nature of type 2 diabetes, aggressive intervention early in the course of the disease, including combination therapy, is often necessary.

Adult↗

Clinical importance of insulin secretion and its interaction with insulin resistance in the treatment of type 2 diabetes mellitus and its complications.

Type 2 diabetes primarily develops from pathogenic defects in the mechanisms of insulin secretion and hepatic and peripheral insulin action. The consequent disruption of normal glucose metabolism involves a number of organ systems and is ultimately manifested in fasting and daytime hyperglycemia. Chronically elevated blood glucose concentrations determine the progression of the disease by further exacerbating insulin resistance and causing beta-cell exhaustion in addition to decreasing their responsiveness to glucose. The beta-cell secretory dysfunction is characterized by the lack of the early phase of glucose-induced insulin secretion and the insufficient and delayed late phase of secretion. Glycemic levels in patients with type 2 diabetes are directly related to the risk of developing microvascular and macrovascular complications, the main cause of the morbidity and mortality associated with this disease. The goal of treatment is to decrease the risk and delay the progression of these complications by improving glycemic control. Current oral antidiabetic agents, used as monotherapy or in combination, include traditional insulin secretagogues, insulin sensitizers and inhibitors of carbohydrate absorption. A greater understanding of the pathophysiology of type 2 diabetes and recent findings on the significance of meal-related glycemia to overall glycemic control are expanding the therapeutic options for treating this disease.

Blood Glucose↗

The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial.

BACKGROUND: A previous paper reported the 6-month comparison of weight loss and metabolic changes in obese adults randomly assigned to either a low-carbohydrate diet or a conventional weight loss diet. OBJECTIVE: To review the 1-year outcomes between these diets. DESIGN: Randomized trial. SETTING: Philadelphia Veterans Affairs Medical Center. PARTICIPANTS: 132 obese adults with a body mass index of 35 kg/m2 or greater; 83% had diabetes or the metabolic syndrome. INTERVENTION: Participants received counseling to either restrict carbohydrate intake to <30 g per day (low-carbohydrate diet) or to restrict caloric intake by 500 calories per day with <30% of calories from fat (conventional diet). MEASUREMENTS: Changes in weight, lipid levels, glycemic control, and insulin sensitivity. RESULTS: By 1 year, mean (+/-SD) weight change for persons on the low-carbohydrate diet was -5.1 +/- 8.7 kg compared with -3.1 +/- 8.4 kg for persons on the conventional diet. Differences between groups were not significant (-1.9 kg [95% CI, -4.9 to 1.0 kg]; P = 0.20). For persons on the low-carbohydrate diet, triglyceride levels decreased more (P = 0.044) and high-density lipoprotein cholesterol levels decreased less (P = 0.025). As seen in the small group of persons with diabetes (n = 54) and after adjustment for covariates, hemoglobin A1c levels improved more for persons on the low-carbohydrate diet. These more favorable metabolic responses to a low-carbohydrate diet remained significant after adjustment for weight loss differences. Changes in other lipids or insulin sensitivity did not differ between groups. LIMITATIONS: These findings are limited by a high dropout rate (34%) and by suboptimal dietary adherence of the enrolled persons. CONCLUSION: Participants on a low-carbohydrate diet had more favorable overall outcomes at 1 year than did those on a conventional diet. Weight loss was similar between groups, but effects on atherogenic dyslipidemia and glycemic control were still more favorable with a low-carbohydrate diet after adjustment for differences in weight loss.

Adolescent↗

Effectiveness of a somatostatin analogue in lowering luteinizing hormone and insulin-stimulated secretion in hyperinsulinemic women with polycystic ovary disease.

OBJECTIVE: To analyze the action of a long-acting somatostatin analogue on circulating insulin levels and on pituitary sensitivity to GnRH in women affected by polycystic ovary disease (PCOD). DESIGN: Controlled clinical study. SETTING: Normal human volunteers in the Department of Obstetrics and Gynecology, Universita' Cattolica del Sacro Cuore. PATIENTS: Twenty euglycemic women affected by PCOD, aged 19 to 30 years, were studied in their early follicular phase. INTERVENTIONS: A long-acting somatostatin analogue (octreotide) was administered SC for 6 weeks; an oral glucose tolerance test (OGTT), a GnRH test, and plasma hormone determinations were performed at baseline and repeated after 6 weeks of treatment. A glucose load also was performed after 1 week of treatment. MAIN OUTCOME MEASURES: Insulin and glucose serum concentrations were measured in all samples under the oral glucose stimulus, LH and FSH were measured under GnRH test. Plasma levels of PRL, sex hormone-binding globulin, androstenedione (A), T, 17 beta-hydroxyprogesterone, DHEAS, and cortisol were measured. Steroids also were assayed after the octreotide administration. RESULTS: Based on the insulin response to OGTT, subjects were classified as hyperinsulinemic (n = 12) and normoinsulinemic (n = 8). Octreotide administration did not affect the glycemic levels in both groups. Octreotide significantly reduced insulin and LH exaggerated response to GnRH stimulus, as well as the A and T circulating levels, only in the hyperinsulinemic group. CONCLUSIONS: A functional linkage exists between exaggerated insulin and LH-stimulated secretion in a group of polycystic ovary patients. Octreotide may be useful in normalizing these alterations and in reducing ovarian androgen secretion of hyperinsulinemic subjects.

Adult↗

Long-term naltrexone treatment reduces the exaggerated insulin secretion in patients with polycystic ovary disease.

OBJECTIVE: To evaluate the involvement of endogenous opiates in the pathophysiology of the hyperinsulinism in patients affected by polycystic ovary disease by administering naloxone and naltrexone. We also studied the hormonal status following long-term opioid antagonist administration. METHODS: Twenty-one women affected by polycystic ovary disease participated in the study. An oral glucose tolerance test (GTT) was performed at baseline and repeated after short-term naloxone infusion and after 6 weeks of naltrexone administration. Plasma glucose and insulin levels were evaluated in all samples. Gonadotropins, sex hormone-binding globulin, and androgen levels were determined initially and after the naltrexone treatment. RESULTS: None of the patients showed any alteration of glucose tolerance. Based on the insulin response to the GTT, the patients were classified as normo- or hyperinsulinemic. Opioid antagonist administration significantly reduced the insulin response to the GTT in hyperinsulinemic patients, without affecting their glycemic levels. In normoinsulinemic patients, glucose plasma levels were increased whereas insulin levels were not modified by the treatments. Gonadotropin and androgen plasma concentrations were not modified after naltrexone administration. CONCLUSIONS: This work supports a role for the endogenous opiates in the regulation of exaggerated insulin secretion in patients with polycystic ovary disease. The reduction of insulin secretion failed to demonstrate any hormonal modification in such hyperandrogenized patients.

Adult↗

Prevention of long-term complications of non-insulin-dependent diabetes mellitus.

Non-insulin-dependent diabetes mellitus (NIDDM) may be the most rapidly-growing chronic disease in the world. Its long-term complications, including retinopathy, nephropathy, neuropathy, and accelerated macrovascular disease cause major morbidity and mortality. Although therapy that normalizes glycemia may prevent the development and delay the progression of long-term complications in NIDDM, as has been demonstrated in insulin-dependent diabetes mellitus (IDDM), no direct data exist to support the efficacy of "intensive therapy" in NIDDM. An alternative approach to preventing the development of long-term complications may be to intervene more distally, i.e., inhibit the mechanism(s) by which elevated glucose levels cause complications. Potential pathogenic mechanisms include the accumulation of sorbitol and other biochemical changes in tissues with aldose reductase, and the modification of proteins by glycation. Pharmacologic probes, including aldose reductase inhibitors and glycation inhibitors such as aminoguanidine, are currently under study and may provide an efficient means of preventing complications, independent of the ambient glycemic level.

Diabetes Mellitus, Type 2↗

Randomized trial of diet versus diet plus cardiovascular conditioning on glucose levels in gestational diabetes.

We studied the impact of a training program on glucose tolerance in gestational diabetes mellitus. Women with gestational diabetes mellitus (N = 19) were randomized into either group I, a 6-week diet alone group (24 to 30 kcal/kg/24 hours; 20% protein, 40% carbohydrate, 40% fat), or group II, which followed the same diet plus exercise (20 minutes three times a week for 6 weeks). An arm ergometer was used to maintain heart rate in the training range. Glycemic response was monitored by glycosylated hemoglobin, a 50 gm oral glucose challenge with a fasting and 1-hour plasma glucose, and blood glucose self-monitoring, fasting and 1 hour after meals. Week 1 glycemic parameters were the same for both groups. Week 6 data (mean +/- SD) were as follows: group I glycosylated hemoglobin, 4.7% + 0.2% versus group II, 4.2% +/- 0.2%; p less than 0.001. The group I glucose challenge fasting value was 87.6 +/- 6.2 versus 70.1 +/- 6.6 mg/dl, p less than 0.001 for group II. The group I 1-hour plasma glucose challenge result was 187.5 +/- 12.9 mg/dl versus 105.9 +/- 18.9 mg/dl for group II, p less than 0.001. The glycemic levels diverged between the groups at week 4. We conclude that arm ergometer training is feasible in women with gestational diabetes mellitus and results in lower glycosylated hemoglobin, fasting, and 1-hour plasma glucose concentrations than diet alone. Arm ergometer training may provide a useful treatment option for women with gestational diabetes mellitus and may obviate insulin treatment.

Blood Glucose↗

[Plasma cortisol and adrenal response to ACTH stimulation in diabetes mellitus with moderate decompensation].

No significant difference was found between the mean plasma cortisol levels in 2 groups of diabetic patients (10 with non-severe metabolic decompensation and 10 well compensated). Likewise, there was not statistical difference on considering the diurnal Cortisol/nocturnal Cortisol quotients in both groups; these quotients besides showed the persistence of the circadian rythm. No valuable difference was seen in the adrenal response to ACTH stimulus. It was found direct correlation between glycemic levels and cortisol increments after stimulus in the total series of 20 patients (r = 0.44; p < 0.05). There were also significant correlations between diurnal and nocturnal Cortisol (r = 0.63; p < 0.01) and between Cortisol levels before and after stimulus (r = 0.68; p < 0.01). No differences were found in Cortisol levels on estimating the incidence of diabetic complications (retinopathy or nephropathy). All these data suggest the tendency to adrenal hyperactivity due to the diabetic decompensation through the action of the hypothalamic-pituitary axis.

Adrenal Glands↗