Severe acute malnutrition may lead both concurrently and subsequently to malabsorption and impaired glucose metabolism from pancreatic dysfunction. We conducted a systematic review to investigate the associations of current and prior postnatal wasting malnutrition with pancreatic endocrine and exocrine functions in humans. We searched PubMed, Google Scholar, Web of Science and reference lists of retrieved articles, limited to articles in English published before 1 February 2022. We included sixty-eight articles, mostly cross-sectional or cohort studies from twenty-nine countries including 592 530 participants, of which 325 998 were from a single study. Many were small clinical studies from decades ago and rated poor quality. Exocrine pancreas function, indicated by duodenal fluid or serum enzymes, or faecal elastase, was generally impaired in malnutrition. Insulin production was usually low in malnourished children and adults. Glucose disappearance during oral and intravenous glucose tolerance tests was variable. Upon treatment of malnutrition, most abnormalities improved but frequently not to control levels. Famine survivors studied decades later showed ongoing impaired glucose tolerance with some evidence of sex differences. The similar findings from anorexia nervosa, famine survivors and poverty- or infection-associated malnutrition in low- and middle-income countries (LMIC) lend credence to results being due to malnutrition itself. Research using large, well-documented cohorts and considering sexes separately, is needed to improve prevention and treatment of exocrine and endocrine pancreas abnormalities in LMIC with a high burden of malnutrition and diabetes.

Other than obesity, no definitive insights have been gained regarding the apparent association between mode of delivery and long-term endocrine and metabolic outcomes in the offspring. We aimed to determine whether elective cesarean delivery (CD) impacts on long-term endocrine and metabolic morbidity of the offspring. A population-based cohort analysis was performed including all singleton-term deliveries occurring between 1991 and 2014 at a single tertiary medical center. A comparison was performed between children delivered via a non-emergent CD and those delivered vaginally (VD). Hospitalizations of the offspring up to the age of 18 years involving endocrine morbidity were evaluated. A Kaplan–Meier survival curve was used to compare cumulative morbidity incidence. Cox and a Weibull regression models were used to control for confounders. During the study period 131,880 term deliveries met the inclusion criteria; 8.9% were elective non-urgent CDs (n=11,768) and 91.1% (n=120,112) were VDs. The survival curve demonstrated a significantly higher cumulative incidence of endo-metabolic morbidity in offspring born via CD (P=0.010). In the regression models, adjusted for maternal obesity, CD was not noted as an independent risk factor for long-term pediatric endocrine and metabolic morbidity of the offspring while maternal obesity emerged as a strong predictor. We therefore conclude that CD per-se does not appear to increase the risk for long-term pediatric endo-metabolic morbidity of the offspring.

The objectives were to conduct a meta-analysis in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards to determine effect sizes (Cohen's d) for cognitive dysfunction in adults with type 2 diabetes, relative to nondiabetic controls, and to obtain effect sizes for the most commonly reported neuropsychological tests within domains. Twenty-four studies, totaling 26,137 patients (n = 3351 with diabetes), met study inclusion criteria. Small to moderate effect sizes were obtained for five of six domains: motor function (3 studies, n = 2374; d = −0.36), executive function (12 studies, n = 1784; d = −0.33), processing speed (16 studies, n = 3076; d = −0.33), verbal memory (15 studies, n = 4,608; d = −0.28), and visual memory (6 studies, n = 1754; d = −0.26). Effect size was smallest for attention/concentration (14 studies, n = 23,143; d = −0.19). The following tests demonstrated the most notable performance decrements in diabetes samples: Grooved Pegboard (dominant hand) (d = −0.60), Rey Auditory Verbal Learning Test (immediate) (d = −0.40), Trails B (d = −0.39), Rey-Osterreith Complex Figure (delayed) (d = −0.38), Trails A (d = −0.34), and Stroop Part I (d = −0.28). This study provides effect sizes to power future epidemiological and clinical diabetes research studies examining cognitive function and to help inform the selection of neuropsychological tests. (JINS, 2014, 20, 1–14)

We describe here the case of a 45-year-old man with a chronic history of heroin abuse who has received methadone maintenance therapy for 12 years. At admission, on this occasion, for stabilisation on methadone, he reported a two-year history of painful gynaecomastia and testicular atrophy. Investigations revealed abnormal sex hormone levels. Liver function tests, thyroid function tests, Brain (pituitary) MRI and viral screens were normal. Following assessment and abnormality in two morning total testosterone level measurements he was diagnosed with hypogonadism secondary to opioid use. Although he had a previous history of alcohol abuse, he was abstinent from alcohol use for five years at time of assessment. He was commenced on parenteral testosterone replacement with therapeutic benefit.

In light of the increased use of opioids, it is important to recognise and manage the endocrine complications of opioid use. The need for an empathic and adequate sexual history, physical examination and investigation is essential in patients who use opioids to ensure that cases of hormonal dysfunction are detected early and managed appropriately.

Parasitism is defined in various ways as an intimate relationship in which one partner, the parasite, lives on or in another, the host, generally at the expense of the latter. Parasitism commonly results in a unique array of host physiological responses and adaptations. Most studies of the physiological effects of parasitism have focused on the pathological consequence of infection and disease. While many physiological changes contribute to pathogenesis, it is now recognized that parasitic infections at sub-clinical levels also produce physiological effects that either ameliorate or may not contribute to the disease process. Moreover, these physiological changes are often manifested by altered host behaviour. Behavioural studies have enabled an ecological- and evolutionary-oriented evaluation of host responses. In this fashion, physiological effects may be assessed as to whether they affect fitness and confer benefit or harm to one or both of the symbionts involved. We briefly examine how these physiological responses, specifically neural, endocrine, neuromodulatory, and immunomodulatory components, may interact to modify host behaviours. We consider the adaptiveness of these responses and how the behavioural patterns elicited may simultaneously appear adaptive for the parasite as well as the host. In addition, we address how parasite-host physiological and behavioural interactions may be altered during the course of parasitism.

Disruption of the endocrine system has been shown to occur in wild freshwater fish populations across the globe. Effects range from subtle changes in the physiology and sexual behaviour of fish to permanently altered sexual differentiation, impairment of gonad development and/or altered fertility. A wide variety of adverse environmental conditions may induce endocrine disruption, including sub-optimal temperatures, restricted food supply, low pH, environmental pollutants, and/or parasites. Furthermore, it is conceivable that any/all of these factors could act simultaneously to cause a range of disparate or inter-related effects. Some of the strongest evidence for a link between an adverse health effect, as a consequence of endocrine disruption, and a causative agent(s) is between the condition of intersex in wild roach (Rutlius rutilus) in UK rivers and exposure to effluents from sewage treatment works. The evidence to indicate that intersex in roach (and other cyprinid fish living in these rivers) is caused by chemicals that mimic and/or disrupt hormone function/balance in treated sewage effluent is substantial. There are a few parasites that affect the endocrine system directly in fish, including the tape worm Ligula intestinalis and a few parasites from the micropsora phylum. L. intestinalis acts at the level of the hypothalamus restricting GnRH secretion (resulting in poorly developed gonads) and is one of the very few examples where an endocrine disrupting event has been shown to result in a population-level effect (reducing it). It is well established that many parasites affect the immune system and thus the most common effect of parasites on the endocrine system in fish is likely to be an indirect one.

Although mating is a necessary prerequisite for the induction of ovulation in the tsetse fly, Glossina morsitans morsitans, neither the accessory gland substance from the male nor any testicular component is responsible for causing ovulation. Experimental evidence suggest that two neural factors, one originating from the uterus during mating act as an afferent stimulus, and the other originating from the ovary during oocyte maturation regulate a cerebral hormonal factor which controls the event of ovulation. It is probable that one successful copulation removes an inhibition for the release of an ovulation stimulating hormone from the neurohemal organ into the circulation. The rate of synthesis and/or transport of the hormone from the neurosecretory cells to the neurohemal organ is probably regulated by the rate of oocyte development.