BackgroundMedical nutrition therapy is recognized as an important treatment option in type 2 diabetes. Most guidelines recommend eating a diet with a high intake of fiber-rich food including fruit. This is based on the many positive effects of fruit on human health. However some health professionals have concerns that fruit intake has a negative impact on glycemic control and therefore recommend restricting the fruit intake. We found no studies addressing this important clinical question. The objective was to investigate whether an advice to reduce the intake of fruit to patients with type 2 diabetes affects HbA1c, bodyweight, waist circumference and fruit intake.MethodsThis was an open randomized controlled trial with two parallel groups. The primary outcome was a change in HbA1c during 12 weeks of intervention. Participants were randomized to one of two interventions; medical nutrition therapy + advice to consume at least two pieces of fruit a day (high-fruit) or medical nutrition therapy + advice to consume no more than two pieces of fruit a day (low-fruit). All participants had two consultations with a registered dietitian. Fruit intake was self-reported using 3-day fruit records and dietary recalls. All assessments were made by the “intention to treat” principle.ResultsThe study population consisted of 63 men and women with newly diagnosed type 2 diabetes. All patients completed the trial. The high-fruit group increased fruit intake with 125 grams (CI 95%; 78 to 172) and the low-fruit group reduced intake with 51 grams (CI 95%; -18 to −83). HbA1c decreased in both groups with no difference between the groups (diff.: 0.19%, CI 95%; -0.23 to 0.62). Both groups reduced body weight and waist circumference, however there was no difference between the groups.ConclusionsA recommendation to reduce fruit intake as part of standard medical nutrition therapy in overweight patients with newly diagnosed type 2 diabetes resulted in eating less fruit. It had however no effect on HbA1c, weight loss or waist circumference. We recommend that the intake of fruit should not be restricted in patients with type 2 diabetes.Trial registrationhttp://www.clinicaltrials.gov; Identifier: NCT01010594.

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The statement that pituitary hyperthyroidism reflects peripheral hyperthyroidism is still controversial. To evaluate a possible relationship between the calcium and the thyroid metabolism, 29 women with thyroxine (T4) substituted hypothyroidism were examined. They were separated into two groups, one with normal (0.15 to 6 mU/l) and one with suppressed TSH (less than 0.15 mU/l). All the women were judged euthyroid both by their T4 and T3 and by their clinics. The daily dose of T4 (median 0.15 mg in both groups) had been unchanged and TSH level had been stable during the previous six months. Bone mineral content (BMC) of the lumbar spine, bone mineral density (BMD) of left and right collum femoris, serum alkaline phosphatase activity (AP), serum concentration of osteocalcin (Ost) and urinary excretion of hydroxyproline/creatine (Hpr/crea) were similar in the two groups. Furthermore, sex- hormone-binding-globulin (SHBG) was equal in the two groups, but significantly higher than in normals (p less than 0.01). A significant positive correlation was found between serum Ost and Hpr/crea (p less than 0.05) indicating a balanced state where bone formation equals bone resorption. AP failed to correlate to Ost and Hpr/crea because the AP raises from both bone and liver of bone and liver metabolism whereas the two others predominantly reflect bone metabolism. SHBG, being a marker of liver metabolism, was elevated in both groups, probably because of the oral administration of T4. Our data suggest that euthyroid, T4 substituted patients have a normal calcium metabolism whether TSH levels are suppressed or not.

A new method for the estimation of the bioavailability of thyroxine (T4) and 3,5,3\m='\-triiodothyronine (T3) is described based on gel separation followed by antibody extraction of labelled T4 and T3 from serum, and using the area under the curve of disappearance of the tracer (AUC) for the calculations. The peak serum concentrations of radioactive labelled T4 and T3 were reached approximately 90 min after oral administration of both tracers. The relative difference of duplicate estimations was below 10% (n = 3). The bioavailability of T4 in 6 euthyroid controls was in median 65% (range 64\p=n-\75%),and it was significantly increased both in hyperthyroidism (88% (75\p=n-\99%), n = 6, P < 0.01) and hypothyroidism (84% (67\p=n-\100%), n = 6, P<0.02).The bioavailability of T3 in 6 euthyroid controls was in median 78% (69\p=n-\99%) and significantly greater than that of T4 (P < 0.02). The bioavailability was unaffected by hyperthyroidism (79% (61\p=n-\98%), n = 9) and hypothyroidism (77% (66\p=n-\97%), n = 7). No significant difference between T4 and T3 bioavailabilities was found in hyper-or hypothyroidism. The clinical implication of the present study is that the bioavailability of T4 and T3 is almost identical and approximately 80% in patients with severe hypothyroidism.Most previous studies on the bioavailability of thy¬ roxine (T4) and 3,5,3'-triiodothyronine (T3) have used the double isotope technique as introduced by Hays (Hays 1968(Hays , 1970Read et al. 1970;Wenzel & Kirschsieper 1977). The bioavailability was calcu¬ lated from the ratio between 125I and 131I labelled iodothyronine as estimated at a time when equilibrium between iv and orally administrated iodo¬ thyronine was assumed. Radioactive labelled iodo¬ thyronine was measured as the total serum radio¬ activity which comprises inorganic iodine, iodoproteins, T4 and T3, and their metabolites. This approach resulted in a considerable variation of individual T4 bioavailability, which was apparently only partly explained by the dose of T4 given, its form of preparation, and whether or not the subjects were fasting (Hays 1968; Wenzel & Kirsch¬ sieper 1977). Only one study had dealt with the bioavailability of T3 and although it generally was found to be high it seemed to decrease from 95 to 79%, 4 and 24 h, respectively, after the administra¬ tion of T3 (Hays 1970).In patients with hyperthyroidism and hypothy¬ roidism T4 bioavailability is comparable to that in controls (Hays 1968;Read et al. 1970) whereas no data are available on the bioavailability of T3 in thyroid disorders.We have evaluated the bioavailability of T4 and T3 in normal subjects and in patients with un¬ treated hyper-and hypothyroidism by estimating the total area under the curve of disappearance (AUC) of radioactive labelled T4 and T3 after simultaneous oral and iv administration. Further¬ more we have isolated the tracers in serum from radioactive iodine, iodoproteins and daughter iodothyronines by means of a technique based on gel separation followed by antibody extraction (Faber et a...

Serum TSH, as measured by a sensitive assay, and serum free T4 and T3, as measured by an ultrafiltration technique, were compared in 14 euthyroid patients with multinodular goiter and 14 normal subjects. T4 and T3 turnover studies also were performed, using the single injection, noncompartmental approach. The goitrous patients had serum free T3 levels within the normal range, but their median serum T3 level was increased compared to that in the normal subjects [goitrous patients, 5.48 pmol/L (range, 4.41-9.03); normal subjects, 4.12 pmol/L (range, 2.58-5.78); P less than 0.01]. The T3 production rate (PR) also was elevated in the patients (median, 39.4 nmol/day X 70 kg; range, 28.7-70.5) compared to that in the normal subjects 31.1 nmol/day X 70 kg; range, 24.4-45.2); P less than 0.05). No differences were found between the two groups with regard to serum free T4 levels or T4 PRs. Serum TSH levels in the patients were reduced (median, 0.20 mU/L; range, less than 0.05-1.6) compared to those in normal subjects (1.8 mU/L; range, 0.36-5.1; P less than 0.01). A significant inverse correlation was found between serum TSH levels and free T3 levels (r = 0.70; P less than 0.001), whereas serum TSH did not correlate with serum free T4 or the PR of T4 or T3. Our data suggest that clinically and biochemically euthyroid patients with multinodular goiter have slight T3 hyperproduction, and TSH secretion in the patients studied was more closely related to serum free T3 levels than to serum free T4 levels or the T3 or T4 PR.