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Increased lipid oxidation is generally observed in subjects with obesity and diabetes and has been suggested to be responsible for the insulin resistance associated with these conditions. We measured, by continuous indirect calorimetry, lipid and glucose oxidation and nonoxidative glucose disposal in 82 obese subjects during a 100-g oral glucose tolerance test (OGTT) and in 26 during a euglycemic insulin (40 mU.min-1.m-2) clamp. The obese subjects were subdivided into those with normal glucose tolerance (group A), those with impaired glucose tolerance (group B), and those with overt diabetes (group C). Forty-five healthy nonobese subjects were subdivided into a young and an older control group, which were age-matched to the nondiabetic obese (groups A and B) and diabetic obese (group C) subjects, respectively. In the postabsorptive state, as well as in response to insulin stimulation (both OGTT and insulin clamp), lipid oxidation was significantly increased in all three obese groups in comparison with either young or older controls. Basal glucose oxidation was significantly decreased in obese nondiabetic and obese glucose--intolerant subjects (groups A and B) compared with age-matched controls. During the OGTT and during the insulin clamp, insulin-stimulated glucose oxidation was decreased in all three obese groups. In contrast, nonoxidative glucose disposal was markedly inhibited in nondiabetic and diabetic obese patients during the euglycemic insulin clamp but not during the OGTT. After glucose ingestion, nonoxidative glucose uptake was normal in nondiabetic obese and glucose-intolerant obese subjects and decreased in diabetic obese subjects. Statistical analysis revealed that lipid and glucose oxidation were strongly and inversely related in the basal state, during euglycemic insulin clamp, and during OGTT. The negative correlation between lipid oxidation and nonoxidative glucose uptake, although significant, was much weaker. Fasting and post-OGTT hyperglycemia were the strongest (negative) correlates of nonoxidative glucose disposal in both single and multiple regression models. We conclude that 1) reduced glucose oxidation and reduced nonoxidative glucose disposal partake of the insulin resistance of nondiabetic obese and diabetic obese individuals; 2) hyperglycemia provides a compensatory mechanism for the defect in nonoxidative glucose disposal in nondiabetic obese subjects; however, this compensation is characteristically lost when overt diabetes ensues; and 3) increased lipid oxidation may contribute, in part, to the defects in glucose oxidation and nonoxidative glucose uptake in obesity.

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Obese persons are often reported to have marked cravings for simple carbohydrate-rich foods. Because of the proposed relationships between protein/carbohydrate selection, plasma tryptophan (TRP) to large neutral amino acids (LNAA) ratios, and brain 5-hydroxytryptamine (5-HT) neurotransmission, we examined the plasma TRP/LNAA ratios in four categories of obese subjects, before and 120 min after oral glucose tolerance test (GTT). Plasma TRP/LNAA ratios were reduced in obese, non-diabetics by 18%, the same extent as for older (approximately 52 yr old) nonobese subjects. In more advanced obesity, ie obesity associated either with glucose intolerance, hyperinsulinemia or hypoinsulinemia, plasma TRP/LNAA ratios were reduced by 25%. One hundred twenty minutes after a 100 g glucose load plasma TRP/LNAA had not been normalized. Based on animal data, these results suggest there may be diminished 5-HT neurotransmission in obese diabetics. The implications of these findings for the cravings of obese for carbohydrate-rich foods is discussed.

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There are three key goals in current management of the diabetic pregnancy. Normal diabetes control before conception and during the first trimester in an attempt to reduce the incidence of congenital abnormalities. This implies that all diabetic women of childbearing age should have counseling before pregnancy. Routine use of new techniques such as home blood glucose monitoring, intensified conventional insulin regimens, or an insulin infusion pump for maintenance of tight metabolic control both before and during pregnancy. Delay in delivery of the baby until the due date, assuming good diabetes control and normal antepartum monitoring of the fetus, to reduce the incidence of macrosomatia, decrease the rate of cesarean section, and decrease neonatal mortality. The current outlook for the pregnant woman with diabetes is an optimistic one. Until recently, most women with diabetes were told that they should avoid pregnancy. Sterilization was often suggested as a means of contraception. Unfortunately, some women are still getting that message from their physician. This is unacceptable, as it is obvious that diabetes is no longer a barrier to pregnancy. Most women with diabetes can now consider the possibility of pregnancy and know that they have a reasonable chance of having a healthy child. Furthermore, new developments in diabetes care continue and should lead to an even brighter future for this group of patients. New advances in treatment, such as implantable insulin pumps, glucose sensors, and islet cell transplants, are just over the horizon. With these developments, a woman with diabetes will be freed from the intensive regimen she must now practice to achieve a successful pregnancy.

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Knowing the relationship between obesity and diabetes, the purpose of our work was to study the alterations in lipid metabolism as measured by continuous indirect calorimetry in the course of a 100-g oral glucose-tolerance test in groups of obese patients without and with diabetes, respectively. Seventy-nine obese patients participated in the study. They were divided into four groups according to the degree of carbohydrate intolerance: group A, normal glucose tolerance; group B, impaired glucose tolerance; group C, diabetes with hyperinsulinemic response to the load; group D, diabetes with impaired insulin response. All four groups of patients presented an increase in lipid oxidation, both in the fasting state and during the three-hour glucose tolerance test, when compared to the control group. The lipid oxidation rate was roughly parallel to plasma free fatty acid (FFA) levels. The contribution of lipids to energy expenditure was higher in obese as compared to control subjects. These observations suggest that the larger part taken by lipids in the energy metabolism of both nondiabetic and diabetic obese humans is a consequence of their increased fat stores and that the resulting decrease in carbohydrate metabolism may lead, as a late consequence, to alterations in glucose tolerance. The latter may result in delayed glucose storage and oxidation in the obese patient.

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In the basal state the body utilizes glucose at a rate of 2.2 - 2.3 mg.kg-1.min-1; of this approximately 1.2 - 1.3 mg.kg-1.min-1 is oxidized, while the remaining 1.0 mg.kg-1.min-1 must be utilized by non-oxidative pathways. Little information is, however, available concerning the insulin dependency of these processes. To examine the role of basal insulin levels on glucose oxidation, glucose storage and total body glucose uptake, somatostatin (10 microgram/min) was infused for 2 h in nine volunteers while maintaining plasma glucose concentration constant at basal levels by an exogenous glucose infusion. Basal plasma insulin fell by about 50% (13 +/- 2 to 7 +/- 1 mU/l, p less than 0.01). Total body glucose metabolism (3H-3-glucose) declined from 2.3 +/- 0.1 to 1.9 +/- 0.1 mg.kg-1.min-1 (p less than 0.01). This decrease was entirely accounted for by a fall in basal glucose oxidation (measured by indirect calorimetry) from 1.3 +/- 0.1 to 0.7 +/- 0.1 mg.kg-1.min-1 (p less than 0.001). To assess the specific role of insulin deficiency in the decline in glucose oxidation, subjects were restudied with somatostatin plus basal insulin replacement (0.07 mg.kg-1.min-1). Fasting insulin concentration (14 +/- 1 mU/l) remained constant during somatostatin plus insulin infusion (13 +/- 1 mU/l) and basal rates of glucose oxidation (1.2 +/- 0.1 mg.kg-1.min-1) and total body glucose uptake did not change significantly. After 2 h, the basal insulin infusion was stopped and somatostatin was continued. Over the subsequent hour, glucose oxidation declined by 0.4 +/- 0.1 mg.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of the present work was to study the effect of a methionine-enkephalin analogue (FK 33-824) on glucose tolerance in man. Groups of 5 to 8 normal subjects were given a 0.5 mg im injection of the drug or placebo just before a 100 g oral glucose load or a 0.5 g/kg iv glucose load. In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. This effect was not observed when glucose was given iv in another group of 5 subjects in whom the significant blunting of the insulin response was accompanied by a significant decrease in glucose tolerance. These observations demonstrate that in man, enkephalin produces a decrease in insulin secretion in response to both oral and iv glucose loads. The absence of any marked impairment in glucose tolerance in the oral test in spite of the decreased insulin response suggests that enkephalin might have an additional effect in delaying glucose absorption.

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The exocrine pancreatic function has been estimated using the N-benzoyl-L-Tyrosyl para-amino-benzoic acid test (NBT PABA test) and by measuring the trypsinemia by radio-immunoassay (RIA trypsinemia) in nonselected cases of Sjögren's syndrome (SS) and seropositive rheumatoid arthritis (RA) in comparison with normal controls. The NBT PABA test was pathological in 37,5% of SS and 35% of RA patients but in none of the controls. The RIA trypsinemia was found to be high in 6,2% of SS and 45% of RA patients. These findings suggest that exocrine pancreatic function is impaired in some SS and RA cases. However, this exocrine pancreatic defect was clinically silent in all patients.

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In this multicentre, between-patient trial the efficacy and tolerability of a cream, containing 0.05% halometasone and 1% triclosan, was compared with those of Nerisona C cream, containing 0.1% diflucortolone valerate and 1% chlorquinaldol, in 183 patients with acute dermatomycoses. Halometasone/triclosan cream and the comparative cream showed closely similar results with respect to good to very good therapeutic effects (60% versus 57%). However, halometasone/triclosan cream proved superior to the comparative preparation with regard to very good (cured) results (53% versus 46%), an early cure in less than 30 days (41% versus 34%) and onset of action within 3 days of starting the treatment (32% versus 18%). Mycological findings were positive on direct microscopy in 36% and 43% and in culture in 19% and 17% of the patients following treatment with halometasone/triclosan cream and the comparative cream preparation, respectively. Adverse effects were reported in seven out of 108 patients treated with halometasone/triclosan cream and in five out of 107 patients treated with the comparative preparation.

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Ornithine-alpha-ketoglutarate (OAK), a drug commonly used in various catabolic states, was studied for its acute effects on endocrine pancreas. A 30-min infusion of OAK (20 g/m2) induced significant increases in insulin levels (from 15 through 60 min) and in glucagon levels (from 15 through 90 min). However, OAK-induced insulin and glucagon responses were lower than after a 0.5 g/kg arginine infusion. The fluctuations of blood glucose levels were much less marked during OAK infusion than during arginine and especially the late fall was less evident.

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