In the mood to be social: Affective state influences facial emotion recognition in healthy adults.

The ability to accurately recognize facial expressions is a key element of social interaction. Facial emotion recognition (FER) assessments show promise as a clinical screening and therapeutic tool, but realizing this potential requires better understanding of the stability of this skill. Transient mood states are known to bias emotion recognition in some contexts and may represent a critical factor impacting FER ability. In particular, it is unclear how natural fluctuations in individuals' mood state over time contribute to specific changes in the ability to recognize facial expressions. The current study tested 55 neurotypical participants across multiple visits using the Emotion Recognition test and found that fluctuations in positive and negative mood state altered recognition of specific emotions. Surprisingly, effects of mood state on emotion recognition were noncongruent; increased positive mood was associated with improved recognition of scared expressions but worsened recognition of happy expressions. Our results suggest that minor fluctuations in mood state in a neurotypical population affect emotion recognition. Therefore, mood should be taken into account by researchers and clinicians assessing FER skills. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Pacemaker function and neural responsiveness of subserosal interstitial cells of Cajal in the mouse colon.

KEY POINTS: Rhythmic action potentials and intercellular Ca2+ waves are generated in smooth muscle cells of colonic longitudinal muscles (LSMC). Longitudinal muscle excitability is tuned by input from subserosal ICC (ICC-SS), a population of ICC with previously unknown function. ICC-SS express Ano1 channels and generate spontaneous Ca2+ transients in a stochastic manner. Release of Ca2+ and activation of Ano1 channels causes depolarization of ICC-SS and LSMC, leading to activation of L-type Ca2+ channels, action potentials, intercellular Ca2+ waves and contractions in LSMC. Nitrergic neural inputs regulate the Ca2+ events in ICC-SS. Pacemaker activity in longitudinal muscle is an emergent property as a result of integrated processes in ICC-SS and LSMC. ABSTRACT: Much is known about myogenic mechanisms in circular muscle (CM) in the gastrointestinal tract, although less is known about longitudinal muscle (LM). Two Ca2+ signalling behaviours occur in LM: localized intracellular waves not causing contractions and intercellular waves leading to excitation-contraction coupling. An Ano1 channel antagonist inhibited intercellular Ca2+ waves and LM contractions. Ano1 channels are expressed by interstitial cells of Cajal (ICC) but not by smooth muscle cells (SMCs). We investigated Ca2+ signalling in a novel population of ICC that lies along the subserosal surface of LM (ICC-SS) in mice expressing GCaMP6f in ICC. ICC-SS fired stochastic localized Ca2+ transients. Such events have been linked to activation of Ano1 channels in ICC. Ca2+ transients in ICC-SS occurred by release from stores most probably via inositol trisphosphate receptors. This activity relied on influx via store-operated Ca2+ entry and Orai channels. No voltage-dependent mechanism that synchronized Ca2+ transients in a single cell or between cells was found. Nitrergic agonists inhibited Ca2+ transients in ICC-SS, and stimulation of intrinsic nerves activated nitrergic responses in ICC-SS. Cessation of stimulation resulted in significant enhancement of Ca2+ transients compared to the pre-stimulus activity. No evidence of innervation by excitatory, cholinergic motor neurons was found. Our data suggest that ICC-SS contribute to regulation of LM motor activity. Spontaneous Ca2+ transients activate Ano1 channels in ICC-SS. Resulting depolarization conducts to SMCs, depolarizing membrane potential, activating L-type Ca2+ channels and initiating contraction. Rhythmic electrical and mechanical behaviours of LM are an emergent property of SMCs and ICC-SS.

The effect of bupropion XL and escitalopram on memory and functional outcomes in adults with major depressive disorder: results from a randomized controlled trial.

Decrements in cognitive function are a common feature of Major Depressive Disorder (MDD), and whether distinct classes of antidepressants differentially affect memory in these individuals has not been sufficiently evaluated. In this study we sought to determine the effect of escitalopram and bupropion XL on memory and psychosocial function. Forty-one individuals (18-50 years) with MDD were enrolled in an 8-week, double-blind, double-dummy, randomized controlled comparative trial of bupropion XL and escitalopram. Thirty-six participants completed pre and post memory assessments. Verbal, non-verbal and working memory were evaluated with a comprehensive neuropsychological battery. Psychosocial function was assessed with the Sheehan Disability Scale and Endicott Work Productivity Scale. Escitalopram and bupropion XL significantly improved immediate as well as delayed verbal and nonverbal memory, global function (all p≤0.001), and work productivity (p=0.045), with no significant between-group differences. Improvement in immediate verbal memory exerted a direct influence on improvement in global function (p=0.006). Treatment with either escitalopram or bupropion XL was associated with improvement in memory and psychosocial function in adults with MDD.

Novel therapeutic targets in depression: minocycline as a candidate treatment.

Mood disorders are marked by high rates of non-recovery, recurrence, and chronicity, which are insufficiently addressed by current therapies. Several patho-etiological models have been proposed that are not mutually exclusive and include but are not limited to the monoamine, inflammatory, neurotrophic, gliotrophic, excitatory, and oxidative stress systems. A derivative of these observations is that treatment(s) which target one or more of these mechanistic steps may be capable of mitigating, or preventing, disparate psychopathological features. Minocycline is an agent with pleiotropic properties that targets multiple proteins and cellular processes implicated in the patho-etiology of mood disorders. Moreover, preclinical and preliminary clinical evidence suggests that minocycline possesses antidepressant properties. Herein, we provide the rationale for conducting a randomized, controlled trial to test the antidepressant properties of minocycline.

Pre-pubertal onset of type 1 diabetes and appearance of retinopathy.

OBJECTIVES: It was suggested that the years of diabetes preceding puberty may not contribute to the development of retinopathy but evidence for this is conflicting. To verify the influence of pre-pubertal diabetes, we compared the correlations between prevalence of retinopathy and diabetes duration in patients who developed type 1 diabetes before and after puberty. METHODS: Six hundred and twenty-eight patients with diabetes onset at age< or =29, on insulin treatment and aged< or =60 at the time of screening for retinopathy were considered retrospectively. Pre-pubertal age was defined as 0-12 in males and 0-11 in females. Two hundred patients had developed diabetes before puberty and 428 after puberty. Screening was by ophthalmoscopy + 35 mm photography or digital photography. RESULTS: Prevalence of retinopathy was lower among patients with pre-pubertal onset and diabetes durations 10-14 and 15-19 years (p=0.006 and p=0.003, respectively) but prevalence rates became similar after 20 yrs duration. CONCLUSION: That retinopathy is infrequent and mild during childhood, is probably due to the short duration of diabetes rather than a specific protective effect of pre-puberty. After 20 years' duration, however, the prevalence of retinopathy is no longer influenced by age at onset, suggesting that, in the longer term, pre-pubertal years do contribute to the onset of retinopathy.

[Diet therapy in non-insulin dependent diabetes mellitus (NIDDM)]. / La dieta nel diabete di tipo II.

The main approach in NIDDM therapy is diet. Most patients present insulin resistance characterized by overweight, VLDL increase, minimal increase of LDL, decrease of HDL cholesterol, and hypertension. The overall goals of nutrition therapy are the maintenance of near normal glucose levels, and the achievement of optimal serum lipid levels with adequate calories for maintaining or attaining a reasonable body weight. In presence of obesity and hypertension even a slightly weight loss could achieve an improvement in metabolic control and in hypertension with a better life expectance. General-ly carbohydrate intake would represent the 50-60% of total caloric amount (with preference to those with low glycemic index), and lipids no more than 35% (less than 10% of these 10-15% from monounsaturated fats with less than 300 mg/day of cholesterol). If elevated very low density lipoproteins level is the primary problem, a beneficial approach is 10% of total caloric intake from saturated fats, 10% from polyunsaturated, and 15-20% from monounsaturated fats with less than 200 mg/day of cholesterol and 40% of carbohydrates. A large amount of fructose (20% of calories) may increase LDL levels but sweeteners as saccarine or aspartame are approved and determine a better diet compliance. Daily consumpion of 20-35 g of dietary fibres from food sources is recommended for metabolic control. Protein intake would be of about 10% of total caloric amount especially in presence of diabetic nepropathy. Alcohol would not exceed 30 g/day for men and 20 g/day for women keeping in mild that alcohol may worsen metabolic control, diet compliance, and may be dangerous itself. For people with hypertension a decrease of dietary sodium intake is recommended. Nutritional recommendations are developed to meet treatment goals and desired outcomes. Monitoring metabolic parameters, blood pressure, and body weight is very important to ensure successful outcomes.

Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.

To determine whether an increased risk for atherosclerosis in older humans is related to changes in postprandial lipoprotein metabolism, we compared the dynamic profiles (0-10 hours) of triglyceride (Tg)-rich lipoproteins and the Tg content in VLDL subfractions in elderly and young subjects after an oral fat load. The plasma Tg response curves displayed significant differences between the groups at all times. Postprandial triglyceridemia was quantified from the plasma response curves as an incremental area, and was significantly different in the two groups (young subjects 231.9 +/- 199.6 vs elderly subjects 511.0 +/- 305.6 mg/dL x 10 hr, p = 0.036). The more scattered VLDL-Tg values were significantly different compared to values at baseline and 6 hours after fat load. Tg baselines in the four VLDL subfractions (expressed as percentages) were higher in the larger particles (B Sf = 175-400) in the elderly subjects, and in the smaller, denser particles (D Sf = 20-100) in the young subjects. In both groups, postprandial hyperlipidemia increased the Tg content of the larger, less dense particles (Sf more than 400), and reduced that of the denser particles. These variations usually coincided with the plasma Tg and VLDL peaks: 63% to 70% above the Tg baseline between the 2nd and 4th hour in all the young subjects: 48% to 68% above the baseline between the 4th and the 6th hour in all the elderly subjects. Total cholesterol variations showed no significant differences between the two groups at any time. All subjects tested for the missense mutation at codon 188 of the human lipoprotein lipase (LPL) gene resulted noncarriers of LPL mutant alleles. Our data show that, after a fatty meal, healthy elderly subjects tend to present prolonged postprandial hypertriglyceridemia, suggesting an atherogenic behavior of their lipid metabolism.

Insulin resistance shows selective metabolic and hormonal targets in the elderly.

There has been no simultaneous evaluation of different aspects of insulin action in ageing. We studied 12 elderly (77 +/- 2 years) and 12 young (26 +/- 1 years) subjects with normal glucose tolerance and matched for sex, body mass index, lean body mass (LBM), blood pressure and physical activity, using a euglycaemic-hyperinsulinaemic clamp at about 350 pmol L-1 in combination with [3H]-glucose infusion. In the elderly group, hepatic glucose production was normal, fasting serum insulin and C-peptide were significantly increased (P = 0.001) and glucose utilization (34.4 +/- 2.4 vs. 44.4 +/- 3.2 mumol kg-1 LBM min-1, P = 0.02) and the percentage maximal suppression of C-peptide (58 +/- 6% vs. 79 +/- 5%, P = 0.02) during the clamp were reduced. Fasting plasma free fatty acid (FFA) and glycerol levels were similar in the two groups, but their percentage maximal suppression during the clamp was reduced in the elderly group (FFA 45 +/- 5% vs. 77 +/- 6%, P = 0.001; glycerol 43 +/- 5% vs. 76 +/- 3%, P = 0.001). Branched-chain amino acids (valine, leucine, isoleucine) and glucagon levels were similar in the two groups, both while fasting and during the clamp. Thus, insulin resistance in ageing appears selective on glucose utilization, inhibition of lipolysis and feedback inhibition of the B-cell secretion.

Comparison of miglitol and glibenclamide in diet-treated type 2 diabetic patients.

The efficacy of the new intestinal alpha-glucosidase inhibitor, miglitol, and glibenclamide were compared in a 6-month double-blind controlled protocol involving 100 non-insulin dependent diabetic patients under diet alone. HbA1c levels (initially between 7 and 11%) were reduced (p < 0.05): -0.78 +/- 0.21% after miglitol and -1.18 +/- 0.20% after glibenclamide. The difference between the two treatments was not significant, although glibenclamide appeared to be more active than miglitol at 8 (p = 0.002) and 16 weeks (p = 0.01) but not at 24 weeks. Fasting glycaemia decreased after miglitol (8.7 +/- 0.3 vs 9.6 +/- 0.3 mmol/l, p = 0.005) and after glibenclamide (8.0 +/- 0.3 vs 9.1 +/- 0.3, p = 0.007). After miglitol, a decrease was noted after breakfast (p < 0.001) and lunch (p < 0.001). The same was true for glibenclamide (p = 0.004 and p < 0.001 respectively). A significant reduction in glucose incremental area during a standard meal test was noted at the end of miglitol (p = 0.008) or glibenclamide treatment (p = 0.04). Subgroups of nonresponders to both treatments were identified (10/49 with miglitol, 9/47 with glibenclamide). Side effects were recorded in 10 patients treated with miglitol (flatulence and meteorism, diarrhoea, 1 discontinued therapy) and in 10 treated with glibenclamide (asthenia, sensation of hunger). This study indicates that miglitol is suitable for initial application in diet-resistant Type 2 diabetic patients, providing, a persistent effect and acceptable side effects.

Metabolic effects of metformin addition to chronic glibenclamide treatment in type 2 diabetes.

In a randomized double-blind cross-over study the addition of metformin to chronic glibenclamide treatment was assessed conventionally (plasma glucose profile and HbA1c measurement) and with an euglycaemic-hyperinsulinaemic glucose clamp in ten non obese (body mass index 22.3 +/- 0.5 (+/- SE)kg.m-2) Type 2 diabetic patients with poor metabolic control. Metformin (500 mg twice a day) or placebo were added in randomized sequence for 6 weeks to their usual sulphonylurea treatment (glibenclamide 5 mg three times a day, before meals). On the last day of each administration period, an euglycaemic (glucose 5.5 +/- 0.5 mmol.l-1), hyperinsulinaemic (insulin 698.1 +/- 22.9 pmol.l-1) clamp was performed, together with a study of insulin binding to circulating monocytes. Metformin reduced fasting glucose levels (6.1 +/- 0.4 vs 6.4 +/- 0.4 mmol.l-1, P = 0.036), mean daily plasma glucose concentrations (9.2 +/- 0.4 mmol.l-1, P < 0.001), and HbA1c (8.7 +/- 0.3 vs 9.3 +/- 0.2%; P = 0.027). No variations were registered in fasting plasma insulin or body weight. A significant reduction of basal hepatic glucose production (12.8 +/- 2.7 vs 33.9 +/- 4.5 mumol.kg-1 min-1, P < 0.001), together with an increase in glucose utilization during the clamp (33.4 +/- 2.8 vs 25.9 +/- 1.1 mumol.kg-1.min-1, P = 0.033), was found after metformin, whereas residual glucose production during insulin infusion did not change. Insulin binding to circulating monocytes was higher after metformin (4.8 +/- 0.9 vs 3.2 +/- 0.6%, P = 0.020), while the lipaemic profile showed a reduction in triglycerides (1.2 +/- 0.1 vs 1.7 +/- 0.3 mmol.l-1, P = 0.039) and an increase in HDL-cholesterol (1.3 +/- 0.1 vs 1.0 +/- 0.1 mmol.l-1, P = 0.004) without variations in total cholesterol. These findings offer further evidence that metabolic control is improved after biguanide addition to sulphonylurea treatment, and support the hypothesis that biguanides improve insulin sensitivity both at the hepatic and peripheral (muscular) levels, as well as triglyceride metabolism.

The artificial endocrine pancreas in clinical practice and research. The present position and future perspectives.

The artificial endocrine pancreas (AEP) is a controlled glucose and/or insulin infusion system in which continuously monitored blood sugar values are fed to a computerised analyser that uses predetermined algorithms to establish the doses to be administered. Since its first appearance in clinical practice and diabetological research during the Sixties, the AEP has been modified in various ways to overcome technical problems associated with the gluco-sensor and algorithms so as to make better use of the glucose-insulin feedback mechanism, and hence obtain a closer correspondence to physiological islet cell activity. As a result of these changes, the AEP can be employed in accordance with the physiopathological principles of insulin secretion in a variety of clinical conditions to secure the short-term control of metabolic alterations in the diabetic. Surgery is one field in which the AEP is used to great advantage, since this and its accompanying anaesthetics are the source of stress, which in turn may result in a rapid and sometimes serious postoperative metabolic derangement, including an increased secretion of anti-insulin hormones. The AEP has also been proposed for diabetic pregnancy and for the treatment of subjects in diabetic coma. It has proved useful in the diagnosis and management of hypoglycaemia due to organic hyperinsulinism, in diabetics with renal failure, in the honeymoon period, and in cases of unstable diabetes. The versatility of its application and its underlying physiopathological principles have enabled the AEP to be predominantly employed in research.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of the metabolic effects of mixed meal and standard oral glucose tolerance test on glucose, insulin and C-peptide response in healthy, impaired glucose tolerance, mild and severe non-insulin-dependent diabetic subjects.

Dietary constituents other than glucose can influence insulin secretion in non-insulin-dependent diabetes mellitus and administration of a standard mixed meal has been proposed as a more physiological test in regard to human diet for evaluating the patient both at the time of diagnosis and during follow-up. This study was carried out to compare the effects of a standard meal and the oral glucose tolerance test on glucose, insulin and C-peptide plasma levels in four groups of subjects: healthy controls, subjects with impaired glucose tolerance, patients with mild non-insulin-dependent diabetes, and non-insulin-dependent diabetic patients with secondary failure to oral agents. Plasma glucose values were significantly higher after the oral glucose tolerance test than after the mixed meal in all four groups of subjects. Plasma insulin and C-peptide values were similar during the two tests in all groups of subjects except in non-insulin-dependent diabetics with secondary failure (flattened curves). Insulin and C-peptide responses per unit rise in blood glucose were significantly higher after the oral glucose tolerance test than after the mixed meal both in mild non-insulin-dependent diabetics (P less than 0.05 and P less than 0.05) and in non-insulin-dependent diabetics in secondary failure (P less than 0.01 and P less than 0.05). There was significant correlation between oral glucose tolerance test and mixed meal glucose incremental areas (r = 0.511, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Double-blind crossover study of acarbose in type 1 diabetic patients.

The addition of acarbose to insulin treatment was evaluated in 14 Type 1 (insulin-dependent) diabetic patients assessed conventionally (blood glucose profile and HbA1c measurement) and with an artificial B-cell. Their metabolic control was poor, fasting blood glucose 10.7 +/- 0.3 (+/- SE) mmol l-1, mean daily blood glucose 9.7 +/- 0.3 mmol l-1, and HbA1c 9.6 +/- 0.2% (normal range 5.0-6.1%). They were of normal body weight (body mass index 22.5 +/- 0.3 kg m-2), and were C-peptide deficient (fasting 0.08 +/- 0.02 nmol l-1). In addition to their usual insulin therapy (46.9 +/- 3.5 U day-1 in three pre-meal injections), they received 100 mg acarbose or placebo three times a day for 6 weeks in a randomized double-blind crossover design. On the last day of either acarbose or placebo treatment, the usual insulin therapy was discontinued and an artificial B-cell was used for insulin delivery, programmed for euglycaemia. Placebo or acarbose was continued before meals. Acarbose reduced mean daily blood glucose concentrations (8.5 +/- 0.3 vs 9.7 +/- 0.3 mmol l-1, p = 0.002) and HbA1c levels (8.3 +/- 0.1 vs 9.6 +/- 0.2%, p less than 0.001). A significant reduction in insulin requirement after meals was found with the artificial B-cell, 25.1 +/- 2.5 (first treatment acarbose) and 24.1 +/- 2.9 U (first treatment placebo) with acarbose and 40.0 +/- 2.5 and 35.6 +/- 2.9 U with placebo (p less than 0.001). These results suggest that acarbose could usefully be administered to Type 1 diabetic patients to ameliorate glucose control and reduce insulin requirement.

Lymphocyte Na,K-ATPase is reduced in aged people.

Na,K-ATPase-dependent 86Rb uptake, maximum velocity (Vmax), Michaelis constant (Km) of the uptake, and [3H]-ouabain binding were investigated in the lymphocytes of 10 elderly subjects (age greater than 60 years), and in 10 middle-aged (41 to 60 years) and 10 young controls (age less than or equal to 40 years). 86Rb uptake was reduced in elderly versus both middle-aged and young subjects (20.14 +/- 3.30 v 35.60 +/- 2.67, P = .002, and v 36.53 +/- 4.49 nmol, P = .012), as was the number of [3H]-ouabain binding sites per cell (32,662 +/- 2,215 v 40,420 +/- 1,184, P = .011, and v 40,596 +/- 1,349, P = .014). Vmax was reduced in elderly v young subjects (1.20 +/- 0.10 v 1.64 +/- 0.13, P = .034), but not versus the middle-age group (1.20 +/- 0.10 v 1.54 +/- 0.12 nmol.min-1, NS). Km was no different among the three groups. No differences were found between middle-aged and young subjects. Significant correlations were observed between age and Na,K-ATPase-dependent 86Rb uptake (r = -.620, P = .00009), Vmax (r = -.439, P = .024), and [3H]-ouabain binding sites (r = -.648, P = .002). Moreover, the site number was positively correlated with both uptake (r = .635, P = .002) and Vmax (r = .554, P = .011). These differences were observed both in women and men. We conclude that there is an age-dependent reduction in lymphocyte Na,K-ATPase activity, which is fully manifested over 60 years, and that this alteration is probably due to the reduced number of functional units of Na,K-ATPase in advancing age.

Lymphocyte (Na,K) ATPase-dependent 86Rb+ uptake in human obesity.

Sodium and potassium ion-activated adenosinetriphosphatase (EC number 3.6.1.3) activity, measured as the uptake of 86 rubidium (an analogue of potassium) was determined on peripheral lymphocytes isolated from 20 normotensive obese subjects and 20 normal weight subjects. No difference in the total uptake of 86Rb or in the Na, K-ATPase-dependent uptake was observed in either group. Furthermore, no correlation between the body mass index (BMI) and the Na,K-ATPase-dependent 86Rb uptake was observed. However the Na,K-ATPase mediated 86Rb uptake was always positively correlated with basal blood insulin levels and the insulin sensitivity index. It may be concluded that no lymphocyte dysfunction of Na,K-ATPase was present in our obese patients and that its activity is controlled by insulin in both normal-weight and obese subjects.

Beta-blockers in hypertensive non-insulin-dependent diabetics: comparison between penbutolol and propranolol on metabolic control and response to insulin-induced hypoglycemia.

In a single blind randomized study the effects of a 4-week administration of propranolol (160 mg/day) and penbutolol (40 mg/day) on metabolic control and insulin-induced hypoglycemia were tested in 8 non-insulin-dependent diabetics with diastolic blood pressure between 95 and 110 mmHg. The recovery from hypoglycemia was not delayed by either drug; hypoglycemic nadir and Conard's K did not change significantly. Symptoms of hypoglycemia were inhibited to a lesser extent and pulse rate decrease was lower after penbutolol vs baseline (65 +/- 2.4 vs 77 +/- 2.4 beats/min, p less than 0.01) than after propranolol vs baseline (61 +/- 1.06 vs 77 +/- 2.4 beats/min p less than 0.001). Both drugs produced similar and significant effects on blood pressure both systolic and diastolic. There were no significant effects on fasting plasma glucose concentration, HbA1c, IRI, urinary C-peptide, triglycerides, total and HDL cholesterol and FFA. IRG decreased after penbutolol vs baseline 60 min after insulin injection (170 +/- 30.8 vs 125 +/- 15.4 pmol/l, p less than 0.05). These results indicate that the use of beta-blockers, in particular penbutolol, for mild to moderate hypertension may be considered the treatment of choice also in non-insulin-dependent diabetics at the therapeutic doses employed.

Effects of sodium and potassium adenosine-triphosphatase on circulating lymphocytes: an approach to human obesity.

The methodological aspects of (Na+, K+)-ATPase-dependent uptake of 86Rb, a potassium analog, were examined on human lymphocytes isolated from peripheral blood. The study of the time-course, the kinetic parameters, i.e., maximum velocity (Vmax) and Michaelis constant (Km) and the ouabain inhibition curve of 86Rb+ uptake confirm that circulating lymphocytes represent a suitable model for the study of (Na+,K+)-ATPase in human diseases. An application to human obesity is reported: the results indicate that 86Rb+ uptake on circulating lymphocytes is similar in obese and non-obese subjects. Therefore, (Na+,K+)-ATPase does not seem to be involved in the pathogenesis of human obesity.

Moderate guar-gum addition to usual diet improves peripheral sensitivity to insulin and lipaemic profile in NIDDM.

The addition of vegetable fibres to the diabetic diet has been reported to ameliorate glycaemic and plasma lipid profiles, and Guar flour seems to obtain the best results. At its usual dose, Guar produces several gastro-intestinal side effects. A lower dose (4 + 4 g/day) was therefore employed in 10 non-insulin dependent diabetics (NIDD). The following parameters were measured at the end of treatment and after a control period: HbA1 levels, hepatic glucose production (3H-Glucose infusion), peripheral sensitivity to insulin and insulin secretion (hyperglycaemic clamp), and specific insulin binding to isolated monocytes. The ultracentrifugal plasma lipid pattern was also measured. No significant body weight change was recorded during the study. A significant glycaemic and insulinaemic decrease in the fasting state was observed after Guar, together with a significant decrease of HbA1 levels (from 8.5 +/- 0.4 to 7.9 +/- 0.4%, p less than 0.05) and amelioration of peripheral sensitivity to insulin (M/I = 14.3 +/- 6.6 versus 24.3 +/- 8.8, p less than 0.025; 50% increase of insulin binding to circulating monocytes) without significant variation of the fasting hepatic glucose production. Decreased B-cell stimulation by flattening post-prandial glycaemic peaks may be an explanation of the reduction of insulin resistance via down-regulation mechanism. As far as the lipid profile is concerned, a significant reduction in total and LDL cholesterol (p less than 0.05 and p less than 0.01) and an increase in HDL-phospholipids (p less than 0.05) were recorded after Guar. These results suggest that Guar in low doses is well accepted and can contribute to a better glycaemic and lipaemic control in NIDDM.