Context Oxytocin (OT) and vasopressin share anatomical pathways of synthesis and secretion, and patients with central diabetes insipidus (CDI) presumably are at risk for OT deficiency. However, an OT-deficient state in hypopituitary patients has not been established. Objectives We hypothesized that men with CDI compared to patients with similar anterior pituitary deficiencies (APD) but no CDI and healthy controls (HC) of similar age and body mass index, would have lower plasma OT levels, associated with increased psychopathology. Design Cross-sectional. Setting Clinical research center. Participants Sixty-two men (20 CDI, 20 APD, 22 HC), age 18 to 60 years. Interventions Frequent sampling of blood every 5 minutes for OT over 1 hour and validated questionnaires to assess psychopathology. Main Outcomes Pooled plasma OT levels; depressive, anxiety, and alexithymia symptoms; and quality of life. Results The mean 1-hour pool of fasting OT levels was lower in CDI compared with APD and HC (P = 0.02 and P = 0.009, respectively), with no differences between APD and HC (P = 0.78). Symptoms of depression, anxiety, and alexithymia were more pronounced in CDI than in HC (P = 0.001, P = 0.004, and P = 0.02, respectively). Although CDI and APD reported worse physical health compared with HC (P = 0.001 and P = 0.005) with no differences between APD and CDI, only CDI reported worse mental health compared with HC (P = 0.009). Conclusions We have demonstrated low plasma OT levels and increased psychopathology in hypopituitary men with CDI, suggestive of a possible OT-deficient state. Larger studies of both sexes are required to confirm these findings and clinically characterize hypopituitary patients with OT deficiency.

Cushing’s syndrome (CS) increases cardiovascular risk (CVR) and adipocytokine imbalance, associated with an increased inflammatory state. Telomere length (TL) shortening is a novel CVR marker, associated with inflammation biomarkers. We hypothesized that inflammatory state and higher CVR in CS might be related to TL shortening, as observed in premature aging. To evaluate relationships between TL, CVR and inflammation markers in CS. In a cross-sectional study, 77 patients with CS (14 males, 59 pituitary-, 17 adrenal- and 1 ectopic-origin; 21 active disease) and 77 age-, gender-, smoking-matched controls were included. Total white blood cell TL was measured by TRF-Southern technique. Clinical data and blood samples were collected (lipids, adrenal function, glucose). Adiponectin, interleukin-6 (IL6) and C-reactive protein (CRP) were available in a subgroup of patients (n=32). Correlations between TL and clinical features were examined and multiple linear regression analysis was performed to investigate potential predictors of TL. Dyslipidemic CS had shorter TL than non-dyslipidemic subjects (7328±1274 vs 7957±1137 bp, p<0.05). After adjustment for age and body mass index, cured and active CS dyslipidemic patients had shorter TL than non-dyslipidemic CS (cured: 7187±1309 vs 7868±1104; active: 7203±1262 vs 8615±1056, respectively, p<0.05). Total cholesterol and triglycerides negatively correlated with TL (r-0.279 and -0.259, respectively, p<0.05), as well as CRP and IL6 (r-0.412 and -0.441, respectively, p<0.05). No difference in TL according the presence of other individual CVR factors (hypertension, diabetes mellitus, obesity) were observed in CS or in the control group. Additional TL shortening was observed in dyslipidemic obese patients who were also hypertensive, compared to those with two or less CVR factors (6956±1280 vs 7860±1180, respectively, p<0.001). Age and dyslipidemia were independent negative predictors of TL. TL is shortened in dyslipidemic CS patients, further worse if hypertension and/or obesity coexist and is negatively correlated with increased inflammation markers. Increased lipids and a “low” grade inflammation may contribute to TL shortening and consequently to premature ageing and increased morbidity in CS.

Context Oxytocin regulates a range of physiological processes including eating behavior and oxytocin administration reduces caloric intake in males. There are few data on oxytocin and eating behavior in healthy females or on the response of endogenous oxytocin to food intake and its relationship to appetite in humans. Objectives To determine the postprandial pattern of oxytocin levels, the relationship between oxytocin and appetite, and the impact of menstrual cycle phase and age on oxytocin levels in females. Design Cross-sectional. Setting Clinical research center. Participants Fifty-five healthy females (age 10 to 45 years). Interventions A standardized mixed meal was administered. Main Outcome Measurements Blood sampling for oxytocin occurred at fasting and at 30, 60, and 120 minutes postmeal. Appetite was assessed using Visual Analogue Scales pre- and postmeal. Results Mean fasting oxytocin levels were 1011.2 ± 52.3 pg/mL (SEM) and decreased at 30 and 60 minutes postmeal (P = 0.001 and P = 0.003, respectively). Mean oxytocin levels decreased19.6% ± 3.0% from baseline to nadir. Oxytocin area under the curve was lower in the early to midfollicular menstrual cycle phase (P = 0.0003) and higher in younger females (P = 0.002). The percent change in oxytocin (baseline to nadir) was associated with postprandial hunger (r_s = -0.291, P = 0.03) and fullness (r_s = 0.345, P = 0.009). These relations remained significant after controlling for calories consumed, menstrual cycle status, and age (P = 0.023 and P = 0.0001, respectively). Conclusions Peripheral oxytocin levels in females decrease after a mixed meal and are associated with appetite independent of menstrual phase, age, and caloric intake, suggesting that endogenous oxytocin levels may play a role in perceived hunger and satiety.

Summary: Telomeres, located at the end of linear chromosomes, are essential to maintain genomic stability. Telomere biology has recently emerged as an important player in the fields of ageing and disease. To maintain telomere length (TL) and reduce its degradation after mitosis, the telomerase enzyme complex is produced. Genetic, epigenetic, hormonal and environmental factors can regulate telomerase function. These include stress hormones such as cortisol and growth factors. The hypothalamic–pituitary–adrenal (HPA) axis has been evaluated in psychiatric diseases where hypercortisolism and oxidative stress are often present. Some researches have linked TL shortening to increases in stress‐related cortisol, but others have not. The effects of cortisol on the telomere system are complex and may depend on the intensity and duration of exposure. On the other hand, low levels of IGF‐1 are associated with inflammation and ageing‐related diseases (ischaemic heart disease, congestive heart failure). Both IGF‐1 and TL diminish with age and are positively and strongly correlated with each other. It is not clear whether this positive correlation reflects a single association or a cause–effect relationship. Further research will ideally investigate longitudinal changes in telomeres and both these hormonal axes. To our knowledge, TL dysfunction has not been described in either endogenous hypercortisolism (Cushing's syndrome) or acromegaly where excessive amounts of GH and consequently IGF‐1 are produced. This review focuses on the possible relationships between telomere dysfunction and the hypothalamic–pituitary–adrenal (HPA) axis and GH‐IGF‐1 system.

Oxytocin (OXT) is a hypothalamic-posterior pituitary hormone with multiple effects, ranging from regulation of energy homeostasis to bone health and psychological well-being, in addition to its well-known effects on labor and lactation. Patients with hypothalamic and pituitary damage have a higher risk for medical and psychiatric comorbidities despite standard-of-care hormone replacement, and a clinically relevant OXT-deficient state has been identified in patients with arginine vasopressin deficiency (formerly known as central diabetes insipidus) in the last decade. Therefore, OXT deficiency in patients with hypothalamic and pituitary damage is an emerging field. While intranasal oxytocin is readily available to patients, it is not Food and Drug Administration approved in the United States and the quality of compounded formulations is unclear. In addition, more research is needed to establish the safety and efficacy of OXT-based therapeutics in patients with hypothalamic and pituitary damage before recommending treatment. This review summarizes the current knowledge of the OXT system, OXT deficiency in other clinical conditions, and relevance to patients with hypothalamic and pituitary damage. We highlight emerging data supporting OXT deficiency in hypothalamic-pituitary disease, diagnostic challenges, development of therapeutic strategies, and future research directions to advance the field.