In four groups of obese patients matched for Body Mass Index (BMI), we studied the effects of different 3-week semi-starvation treatments followed by an 8-week hypocaloric (1008 kcal, protein 20%, carbohydrate 40%) diet with or without low doses of T3 therapy. Dietary intake (formula diet) in the semi-starvation period was 480 kcal, with 66 g protein (P) and 51 g carbohydrate (CHO) in groups I and III and with 33 g P and 84 g CHO in groups II and IV. Moreover, groups III and IV were given low doses (20 micrograms twice a day) of T3 while groups I and II received a placebo. During semi-starvation periods, a similar fall in BMI values was found in all groups, while during the low-calorie diet, T3-treated patients showed the greater BMI reduction. During semi-starvation, nitrogen balance was significantly more negative in low-protein than in high-protein-treated groups; differences between T3-treated (III and IV) and control (I and II) groups were not significant over this relatively short treatment period. No differences in 24 h urinary 3-methylhistidine or alanine excretion were evident between the four groups. During the entire period of study, daily urine creatinine excretion did not change in any group. In conclusion, in our study low-dose T3 therapy was seen to favour weight loss during low-calorie diet although negative effects on protein metabolism were not excluded, particularly when relatively small amounts of protein were administered.

Relationships between iodothyronine and metabolic substrate metabolism during undernutrition were evaluated in four normal subjects who fasted for 48h (Group I) and in four groups (II to V) of obese patients who underwent selective dietary manipulations: 360 calories [carbohydrate (CHO) 40 g/day]; 800 calories containing respectively 19 g/day - ketogenic - (K) and 112 g/day - non ketogenic - (NK) of CHO; and a step-diet programme (during which total calories were progressively reduced from 2500 to 500). Serum T3 levels decreased significantly and constantly during fasting, 360 and 800 K studies, and transiently during the 800 NK diet. During the step-diet programme, a significant fall was found only when 1250 K or less were given. Conversely, serum reverse T3 rose significantly and constantly during 360 and 800 K diets, while a transient increase was found during the 800 NK diet. During the step-diet programme reverse T3 rose only when 750 calories were given. Ketogenesis developed in all studies but one (800 NK), and in the step-diet programme significantly below the 1000 calorie step. Other substrate modifications in each study were also evaluated. Serum T3 levels showed a significant correlation with ketone bodies (KB) in all the ketogenic studies, while no correlation was found in non ketogenic study (800 NK). During the step-diet programme ketone bodies and iodothyronine modifications appeared to be related to the amount of calories. Based on these results, we suggest a relationship between the dietary-induced modifications of iodothyronine metabolism and the development of ketogenesis.

The effect of different hypocaloric carbohydrate (CHO) intakes was evaluated in 8 groups of obese patients in order to assess the role of the CHO and the other dietary sources in modulating the peripheral thyroid hormone metabolism. These changes were independent of those of bw. Serum T3 concentrations appear to be more easily affected than those of reverse T3 by dietary manipulation and CHO content of the diet. A fall in T3 levels during the entire period of study with respect to the basal levels occurred only when the CHO of the diet was 120 g/day or less, independent of caloric intake (360, 645 or 1200 calories). Moreover, reverse T3 concentrations were found increased during the entire period of study when total CHO were very low (40 to 50 g/day) while they demonstrated only a transient increase when CHO were at least 105 g/day (with 645 or more total calories). Indeed, our data indicate that a threshold may exist in dietary CHO, independent of caloric intake, below which modifications occur in thyroid hormone concentrations. From these results it appears that the CHO content of the diet is more important than non-CHO sources in modulating peripheral thyroid hormone metabolism and that the influence of total calories is perhaps as pronounced as that of CHO when a "permissive" amount of CHO is ingested.

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In this study, we evaluated in normal subjects, insulin-dependent (IDD) and non-insulin-dependent (NIDD) diabetics, the diurnal urinary C-peptide excretion rate (CPR-U) and its relationship to serum C-peptide concentration and glucose:C-peptide molar ratio, and to the common parameters of metabolic control. The CPR-U (and CPR-U/g creatinine) were significantly lower in IDD and higher in NIDD compared to control subjects. Moreover, a good and significant correlation with serum C-peptide concentrations and the glucose:C-peptide ratio in diabetic subjects as well as in controls and diabetics considered together was found. A slight but significant correlation was present in diabetic subjects between CPR-U and body mass index (r = 0.45), 24-h glycosuria (r = 0.36), HbA1 levels (r = 0.31), post-prandial glucose concentrations (r = 0.26) and per cent glucose variation after each meal (r = 0.34). No differences were found in CPR-U and the degree of metabolic control between obese and non-obese NIDD. In conclusion, CPR-U may be a useful and simple method of defining the secretory activity of the B-cell. Metabolic control in diabetics is slightly correlated to the degree of B-cell function as evaluated by the diurnal excretion rate of C-peptide in urine.