ABSTRACT
BACKGROUND: In a preliminary report, we found an association between hyperinsulinemia in the basal (fasting) state and the development of diabetes. OBJECTIVES: The current analysis further explored the long term link between basal hyperinsulinemia and conversion to dysglycemia. METHODS: This is a prospective study with up to 24 years of follow-up of 515 normoglycemic individuals (mean age at follow up = 70.3 ± 7.0; range 58-94) of an Israeli cohort. Fasting glucose and insulin were measured, and dysglycemia was defined as fasting glucose > 100 mg/dL. RESULTS: At the end of the follow-up period, almost half had progressed to dysglycemia. Male sex and elevated baseline levels of basal insulin, body mass index, blood glucose and blood pressure each favoured progression to dysglycemia over the subsequent two decades. A multivariate logistic regression model identified basal hyperinsulinemia as the strongest predictor for progression to dysglycemia (odds ratio = 1.79; 95% confidence interval 1.12-2.88), while controlling for ethnicity, blood pressure, fasting glucose, male sex, body mass index and age. CONCLUSIONS: Basal hyperinsulinemia in normoglycemic adults constitutes an independent risk factor for metabolic deterioration to dysglycemia over adulthood, and may help to identify apparently healthy subjects at increased risk for diabetes.
Subject(s)
Hyperinsulinism/physiopathology , Insulin/blood , Prediabetic State/etiology , Adult , Blood Glucose/analysis , Body Mass Index , Cohort Studies , Disease Progression , Early Diagnosis , Fasting/blood , Female , Follow-Up Studies , Humans , Hyperinsulinism/blood , Israel , Male , Middle Aged , Prediabetic State/blood , Prediabetic State/diagnosis , Prospective Studies , Risk Factors , Sex CharacteristicsABSTRACT
The rising prevalence of obesity has reached pandemic proportions, with an associated cost estimated at up to 7% of health expenditures worldwide. Bariatric surgery is currently the only effective long-term treatment for obesity and obesity-related co-morbidities in clinically severely obese patients. However, the precise physiological mechanisms underlying the postsurgical reductions in caloric intake and body weight are poorly comprehended. It has been suggested that changes in hormones involved in hunger, food intake and satiety via the neurohormonal network may contribute to the efficacy of bariatric procedures. In this review, we consider how gastrointestinal hormone concentrations, involved in appetite and body weight regulation via the gut-brain axis, are altered by different bariatric procedures. Special emphasis is placed on neurohormonal changes following Roux-en-Y gastric bypass surgery, which is the most common and effective procedure used today.
