Minerva Endocrinologica 

About: Minerva Endocrinologica is an academic journal published by Edizioni Minerva Medica. The journal publishes majorly in the area(s): Diabetes mellitus & Thyroid. It has an ISSN identifier of 0391-1977. Over the lifetime, 1075 publications have been published receiving 11393 citations.

Stress and eating behaviors.

Abstract: Obesity is a heterogeneous construct that, despite multiple and diverse attempts, has been difficult to treat. One conceptualization gaining media and research attention in recent years is that foods, particularly hyperpalatable (e.g., high-fat, high sugar) ones, may possess addictive qualities. Stress is an important factor in the development of addiction and in addiction relapse, and may contribute to an increased risk for obesity and other metabolic diseases. Uncontrollable stress changes eating patterns and the salience and consumption of hyperpalatable foods; over time, this could lead to changes in allostatic load and trigger neurobiological adaptations that promote increasingly compulsive behavior. This association may be mediated by alterations in the hypothalamic-pituitary-adrenal (HPA) axis, glucose metabolism, insulin sensitivity, and other appetite-related hormones and hypothalamic neuropeptides. At a neurocircuitry level, chronic stress may affect the mesolimbic dopaminergic system and other brain regions involved in stress/motivation circuits. Together, these may synergistically potentiate reward sensitivity, food preference, and the wanting and seeking of hyperpalatable foods, as well as induce metabolic changes that promote weight and body fat mass. Individual differences in susceptibility to obesity and types of stressors may further moderate this process. Understanding the associations and interactions between stress, neurobiological adaptations, and obesity is important in the development of effective prevention and treatment strategies for obesity and related metabolic diseases.

Glucocorticoids, stress, and fertility.

Abstract: Modifications of the hypothalamo-pituitary-adrenal axis and associated changes in circulating levels of glucocorticoids form a key component of the response of an organism to stressful challenges. Increased levels of glucocorticoids promote gluconeogenesis, mobilization of amino acids, and stimulation of fat breakdown to maintain circulating levels of glucose necessary to mount a stress response. In addition to profound changes in the physiology and function of multiple tissues, stress and elevated glucocorticoids can also inhibit reproduction, a logical effect for the survival of self. Precise levels of glucocorticoids are required for proper gonadal function; where the balance is disrupted, so is fertility. Glucocorticoids affect gonadal function at multiple levels in hypothalamo-pituitary-gonadal axis: 1) the hypothalamus (to decrease the synthesis and release of gonadotropin-releasing hormone [GnRH]); 2) the pituitary gland (to inhibit the synthesis and release of luteinizing hormone [LH] and follicle stimulating hormone [FSH]); 3) the testis/ovary (to modulate steroidogenesis and/or gametogenesis directly). Furthermore, maternal exposure to prenatal stress or exogenous glucocorticoids can lead to permanent modification of hypothalamo-pituitary-adrenal function and stress-related behaviors in offspring. Glucocorticoids are vital to many aspects of normal brain development, but fetal exposure to superabundant glucocorticoids can result in life-long effects on neuroendocrine function. This review focuses on the molecular mechanisms believed to mediate glucocorticoid inhibition of reproductive functions and the anatomical sites at which these effects take place.

Neuropsychiatric aspects of hypothyroidism and treatment reversibility. .

Abstract: Thyroid hormone has important actions in the adult brain, and it is well accepted that hypothyroidism is associated with neuropsychiatric complaints and symptoms. Neuropsychiatric symptoms refer to a spectrum of emotional and cognitive problems that are directly related to changes in the brain secondary to multiple factors, including the direct effects of thyroid disease, as well as hormone deprivation in brain tissue. Hypothyroidism impacts aspects of cognitive functioning and mood. More severe hypothyroidism can mimic melancholic de-pression and dementia. Neuropsychiatric symptoms tend to improve with treatment and normalization to a euthyroid state, though the pattern is inconsistent and complete recovery is uncertain. The degree to which mild hypothyroidism, or subclinical hypothyroidism (SCH), impacts mood and cognitive functions and whether these symptoms respond to treatment, remains controversial. Most studies support a relationship between thyroid state and cognition, particularly slowed information processing speed, reduced efficiency in executive functions, and poor learning. Furthermore, hypo-thyroidism is associated with an increased susceptibility to depression and reductions in health-related quality of life. Controlled studies suggest that cognitive and mood symptoms improve with treatment, though the data are equivocal and limited by diverse methodologies. Functional neuroimaging data provide support for the mood and cognitive findings and treatment reversibility for both overt and SCH. These findings are not, however, without controversy. Recent investigations into the impact of SCH on cognition and mood, coupled epidemiological studies investigating the normal spectrum of thyroid stimulating hormone, have fueled significant debate regarding the appropriate, healthy range for TSH levels. This has led to concern over whether patients with overt hypothyroidism may be undertreated and whether SCH patients are truly out of the range of normal thyroid functioning and should be treated. The following is a review of the extant literature on the impact of hypothyroidism on cognition and mood, reversibility of symptoms, and treatment approaches. The spectrum of thyroid disease is reviewed, but mild, or subclinical, hypothyroidism is emphasized. The potential role of autoimmunity in neuropsychiatric symptoms and treatment resistance is addressed. Limitations of the current literature and future directions are discussed.

Adipose tissue, obesity and non-alcoholic fatty liver disease.

Abstract: The association of obesity with non-alcoholic fatty liver disease (NAFLD) has been established. Obesity has been linked not only to initial stages of the disease, i.e., simple steatosis (SS), but also to its severity. From an epidemiologic point of view, both diseases has an increasing prevalence worldwide. From a pathogenetic point of view, obesity and its associate IR contribute to the initial fat accumulation in the hepatocyte (SS), but also to the progression of SS to nonalcoholic steatohepatitis (NASH), NASH-related cirrhosis and hepatocellular carcinoma (HCC). From a clinical point of view, obesity has increased morbidity and mortality when combined with NAFLD, owing to cardiovascular and liver-specific mortality, including higher HCC risk. From a therapeutic point of view, weight loss is regarded as the cornerstone for the disease prevention and treatment. Although diet and exercise are the first choice to this aim, they are both difficult to achieve and sustain. Thus, the need for pharmacological treatment is considered of high importance. To treat obesity through pharmacologic weight loss, orlistat has been investigated, though with limited efficacy. Currently, liraglutide appears to be more efficacious, but it has not been officially approved for specifically NASH patients. Bariatric surgery is another alternative for severely obese patients showing histological improvement in NASH patients. However, since relative data from randomized trials are very limited, morbid obesity-related NASH patients may be subjected to bariatric surgery only after a careful individualized risk-benefit assessment.

Diabetes and the hypothalamo-pituitary-adrenal (HPA) axis.

Abstract: Patients and animals with poorly controlled or uncontrolled diabetes present with diurnal hypersecretion of glucocorticoids and altered regulation of the hypothalamo-pituitary-adrenocortical (HPA) axis. Although some of these changes are reversed with insulin replacement therapy, neuroendocrine function is not always restored to normal, even with rigorous glycemic control. In addition, stress responsiveness is also impaired in diabetes and this has important implications in the way patients with diabetes cope with many stress challenges, including the metabolic challenge of insulin-induced hypoglycemia. HPA dysregulation in diabetes appears to involve complex interactions between impaired glucocorticoid negative feedback sensitivity and factors such as hypoinsulinemia, hyperglycemia and/or hypoleptinemia, that may increase central drive of the axis. This review examines some of the evidence indicating hyperactivation of the HPA axis in patients with diabetes. Using the streptozotocin-diabetic rat as a model of type-1 diabetes, we will focus on elucidating some of the mechanisms underlying HPA dysregulation in diabetes. Hyperactivation of the HPA axis in diabetes is associated with increased expression of hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal mineralocorticoid receptor (MR) mRNA. Although insulin replacement restores ACTH and corticosterone levels to normal, likely through glucocorticoid-mediated suppression of ACTH secretion, CRH and MR mRNA expression remain elevated. A better understanding of these mechanisms may be important in developing new treatment modalities for patients with diabetes mellitus.