Growth hormone (GH) plays a key role not only in the promotion of linear growth but also in the regulation of intermediary metabolism, body composition, and energy expenditure. On the whole, the ...hormone appears to direct fuel metabolism towards the preferential oxidation of lipids instead of glucose and proteins, and to convey the energy derived from metabolic processes towards the synthesis of proteins. On the other hand, body energy stores and circulating energetic substrates take an important part in the regulation of somatotropin release. Finally, central and peripheral peptides participating in the control of food intake and energy expenditure (neuropeptide Y, leptin, and ghrelin) are also involved in the regulation of GH secretion. Altogether, nutritional status has to be regarded as a major determinant in the regulation of the somatotropin–somatomedin axis in animals and humans. In these latter, overweight is associated with marked impairment of spontaneous and stimulated GH release, while acute dietary restriction and chronic undernutrition induce an amplification of spontaneous secretion together with a clear-cut decrease in insulin-like growth factor I (IGF-I) plasma levels. Thus, over- and undernutrition represent two conditions connoted by GH hypersensitivity and GH resistance, respectively. Anorexia nervosa (AN) is a psychiatric disorder characterized by peculiar changes of the GH–IGF-I axis. In these patients, low circulating IGF-I levels are associated with enhanced GH production rate, highly disordered mode of somatotropin release, and variability of GH responsiveness to different pharmacological challenges. These abnormalities are likely due not only to the lack of negative IGF-I feedback, but also to a primary hypothalamic alteration with increased frequency of growth hormone releasing hormone discharges and decreased somatostatinergic tone. Given the reversal of the above alterations following weight recovery, these abnormalities can be seen as secondary, and possibly adaptive, to nutritional deprivation. The model of AN may provide important insights into the pathophysiology of GH secretion, in particular as regards the mechanisms whereby nutritional status effects its regulation.
ObjectiveWe previously described in young thalassaemic patients an altered cortisol and ACTH responsiveness suggesting an impaired adrenocortical reserve. Owing to iron overload, a worsening of ...adrenal function should be expected in adult patients.DesignIn 124 adults with β-thalassaemia, urinary free cortisol (UFC) and plasma ACTH levels were determined and compared with those measured in 150 controls. In 45 patients, cortisol was measured in response to: i) tetracosactide 1 μg as an i.v. bolus (low-dose test, LDT) and ii) tetracosactide 250 μg infused i.v. over 8 h (high-dose test, HDT).ResultsUFC and serum cortisol were within the reference range in all patients. Conversely, basal plasma ACTH values were above the upper limit of the normal range in 19 patients. There were no statistically significant differences in the mean values of UFC, basal serum cortisol and plasma ACTH between patients and controls. A subnormal cortisol response to the LDT was registered in 18 out of 56 patients. Three of these patients also displayed a subnormal response to the HDT, together with elevated baseline plasma ACTH levels. In the LDT, a positive correlation was found between basal and peak cortisol values (P<0.0001). The latter were negatively correlated with basal ACTH values in both LDT (P<0.0001) and HDT (P<0.0001).ConclusionsAdult thalassaemic patients often present a subtle impairment of adrenocortical function. This may become clinically relevant in case of major stressful events. Thus, we recommend an assessment of adrenocortical function in all adult thalassaemic patients.
BackgroundThe diagnosis of GH deficiency (GHD) in obese patients is complicated by the reduced GH secretion associated with overweight. A GH response to GHRH+arginine lower than 4.2 μg/l is currently ...considered indicative of GHD in obesity. The aim of the study was to investigate the effect of acute pharmacological blockade of lipolysis on the GH response to GHRH+arginine in obese patients.Patients and methodsTwo groups of patients were studied: 12 obese patients with proven GHD and 14 patients with essential obesity. On separate occasions, two tests were carried out in each patient: GHRH+arginine and GHRH+arginine preceded by acipimox.ResultsThe mean GH peak after GHRH+arginine was significantly lower in hypopituitary patients than in subjects with essential obesity. Acipimox significantly increased the mean GH response in patients with essential obesity, but not in hypopituitary subjects. All hypopituitary patients and 7/14 patients with essential obesity displayed GH peaks lower than 4.2 μg/l after GHRH+arginine: the GH response to the test increased after acipimox pretreatment in five of these seven essentially obese subjects. After acipimox administration, free fatty acids (FFAs) significantly fell in both groups with comparable mean absolute decreases. All IGF1 values were normal in both groups of subjects.ConclusionsOur study has demonstrated that the acipimox-induced acute reduction of circulating FFA levels increases mean somatotropin response to GHRH+arginine in patients with essential obesity, whereas it has no effect in hypopituitary subjects. The current criterion for the diagnosis of GHD in obese patients may be misleading. Indeed, subjects affected by third degree obesity, like most of our patients, may be erroneously classified as really GH-deficient and started on an expensive unjustified treatment. It appears therefore that the current criteria for the diagnosis of GHD in obesity should be reconsidered in the light of further studies also taking into account different body mass index groups.
Vitamin D is a pro-hormone belonging to the category of the fat-soluble group of vitamins; it is obtained more from solar exposure and in smaller quantities through feeding. Although vitamin D has ...traditionally been shown to be involved in calcium homeostasis and bone health, recent studies have found a positive association between vitamin D and sleep. In particular, clinical studies in humans indicate that low levels of vitamin D are correlated with poor quality and short sleep duration. The mechanism by which this association is explained is still unclear. However, vitamin D receptors have been found in the brain regions involved in sleep regulation, and vitamin D appears to be involved in regulating the sleep–wake cycle. The current review summarizes the available evidence regarding the association between vitamin D and sleep, focusing on both clinical and preclinical studies.
•Low levels of vitamin D are correlated with poor quality sleep and short sleep duration.•Vitamin D receptors have been found in the brain regions involved in sleep regulation.•Vitamin D regulates the sleep–wake cycle.
High carbohydrate intake and low-grade inflammation cooperate with insulin resistance and hyperandrogenism to constitute an interactive continuum acting on the pathophysiology of polycystic ovary ...syndrome (PCOS), the most common endocrine disorder in women of reproductive age characterised by oligo-anovulatory infertility and cardiometabolic disorders. The role of insulin in PCOS is pivotal both in regulating the activity of ovarian and liver enzymes, respectively involved in androgen production and in triggering low-grade inflammation usually reported to be associated with an insulin resistance, dyslipidaemia and cardiometabolic diseases. Although an acute hyperglycaemia induced by oral glucose loading may increase inflammation and oxidative stress by generating reactive oxygen species through different mechanisms, the postprandial glucose increment, commonly associated with the Western diet, represents the major contributor of chronic sustained hyperglycaemia and pro-inflammatory state. Together with hyperinsulinaemia, hyperandrogenism and low-grade inflammation, unhealthy diet should be viewed as a key component of the ‘deadly quartet’ of metabolic risk factors associated with PCOS pathophysiology. The identification of a tight diet–inflammation–health association makes the adoption of healthy nutritional approaches a primary preventive and therapeutic tool in women with PCOS, weakening insulin resistance and eventually promoting improvements of reproductive life and endocrine outcomes. The intriguing nutritional–endocrine connections operating in PCOS underline the role of expert nutritionists in the management of this syndrome. The aim of the present review is to provide an at-a-glance overview of the possible bi-directional mechanisms linking inflammation, androgen excess and carbohydrate intake in women with PCOS.
•The relationship between taste perception and eating disorders was investigated.•Taste impairments occurred differently in obese subjects with eating disorders.•Subjects with mixed eating disorders ...shown a reduced perception of salty stimuli.•Emotional and external eating characterized obese with eating disorders.•Targeting taste might be a promising strategy to personalize the dietary approach.
Eating disorders (i.e., food addiction and binge eating) are a significant cause of morbidity and mortality and are considered one of the most common underlying causes of weight loss failure. Despite ongoing efforts to better understand dysregulated eating, the core phenomenon of the mechanisms underlying the perception of food properties and the possible sensory deficits in eating disorders remains scarcely investigated. This is surprising as the perception of food plays a central role in choosing what we eat and could be relevant in maintaining disordered eating behaviours in patients with obesity. To address this knowledge gap, we tested the hypothesis that taste response profiles are differentially linked to nutritional status and eating disorder types. In addition, a range of eating behavioural attitudes associated with over-consumption was also evaluated to assess their importance in driving abnormal eating. One hundred and twenty-two patients with obesity were studied (37 simple obese; 43 obese with food addiction; 42 obese with co-occurring food addiction and binge eating). Forty-three subjects were recruited as the control group. Sweet and salty taste thresholds (target stimuli associated with binge/compulsive eating) were measured with the 3-Alternative-Forced-Choice method, and eating habits (external, emotional, and restrained eating) were assessed by the Dutch Eating Behaviour Questionnaire.
Results generally showed that patients with obesity (with and without eating disorders) presented a significantly (p < 0.001) lower acuity to sweet and salty tastes compared to controls. In particular, patients with co-occurring food addiction and binge eating showed the highest salty threshold compared to the other groups. Moreover, this group had significantly (p < 0.001) higher emotional and external eating scores than the others.
Our data suggest that targeting taste might be a novel approach toward weight control to prevent the risk of therapeutic failure, identify new intervention strategies and, above all, personalise the type of dietary approach to be adopted with the obesity endophenotype.
Eating is a multisensory behavior. The act of placing food in the mouth provides us with a variety of sensory information, including gustatory, olfactory, somatosensory, visual, and auditory. ...Evidence suggests altered eating behavior in obesity. Nonetheless, multisensory integration in obesity has been scantily investigated so far. Starting from this gap in the literature, we seek to provide the first comprehensive investigation of multisensory integration in obesity. Twenty male obese participants and twenty male healthy-weight participants took part in the study aimed at describing the multisensory temporal binding window (TBW). The TBW is defined as the range of stimulus onset asynchrony in which multiple sensory inputs have a high probability of being integrated. To investigate possible multisensory temporal processing deficits in obesity, we investigated performance in two multisensory audiovisual temporal tasks, namely simultaneity judgment and temporal order judgment. Results showed a wider TBW in obese participants as compared to healthy-weight controls. This holds true for both the simultaneity judgment and the temporal order judgment tasks. An explanatory hypothesis would regard the effect of metabolic alterations and low-grade inflammatory state, clinically observed in obesity, on the temporal organization of brain ongoing activity, which one of the neural mechanisms enabling multisensory integration.
Abstract
Preliminary evidence showed a reduced temporal sensitivity (i.e., larger temporal binding window) to audiovisual asynchrony in obesity. Our aim was to extend this investigation to ...visuotactile stimuli, comparing individuals of healthy weight and with obesity in a simultaneity judgment task. We verified that individuals with obesity had a larger temporal binding window than healthy-weight individuals, meaning that they tend to integrate visuotactile stimuli over an extended range of stimulus onset asynchronies. We point out that our finding gives evidence in support of a more pervasive impairment of the temporal discrimination of co-occurrent stimuli, which might affect multisensory integration in obesity. We discuss our results referring to the possible role of atypical oscillatory neural activity and structural anomalies in affecting the perception of simultaneity between multisensory stimuli in obesity. Finally, we highlight the urgency of a deeper understanding of multisensory integration in obesity at least for two reasons. First, multisensory bodily illusions might be used to manipulate body dissatisfaction in obesity. Second, multisensory integration anomalies in obesity might lead to a dissimilar perception of food, encouraging overeating behaviours.
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Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
General rates of over- and underreplacement in levothyroxine (LT4) users with primary hypothyroidism are variably high. No information on LT4 adequacy exists in obesity.
We explored rates and factors ...relating to LT4 adequacy in obese patients with primary hypothyroidism.
Tertiary care center.
Among 4954 consecutive obese patients admitted between 2011 and 2014, 691 hypothyroid patients receiving LT4 therapy and 691 body mass index (BMI)-, age-, and sex-matched euthyroid controls underwent analysis of thyroid function, glucolipid profile, body composition, and indirect calorimetry. LT4 users were classified into low TSH (<0.27 mU/L), euthyroid (0.27 to 4.2 mU/L), and high TSH (>4.2 mU/L).
LT4 users constituted 13.9% of the incident population. TSH was low in 7.5%, high in 17.2%, and normal in 75.2% of LT4 users. Overtreatment decreased with aging and more LT4 users ≥65 years of age had normal TSH than those <65 years of age (P < 0.05). Compared with the euthyroid obese group, LT4 users showed higher adiposity, similar insulin resistance, but a healthier lipid profile. In multivariable analyses, LT4 dose was predicted by fat-free mass, hypothyroidism cause, and sex (P < 0.0001 to < 0.05). Risk of LT4 overreplacement increased with younger age (OR 0.96; 95% CI 0.94 to 0.99), higher LT4 dose (OR 2.98; 95% CI 1.44 to 6.14), and lower BMI (OR 0.93; 95% CI 0.88 to 0.99). Male sex increased the likelihood of LT4 underreplacement (OR 2.37; 95% CI 1.10 to 5.11).
Obesity is associated with milder rates of inadequate LT4 treatment compared with nonobese populations. LT4 adequacy increases with aging. Age, body composition, and sex are main determinants of LT4 requirements in obesity.
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