Beta-cell function and visceral fat in lactating women with a history of gestational diabetes

Lack of association of liver fat with model parameters of β-cell function in men with impaired glucose tolerance and type 2 diabetes

“…Recently, we reported that fat localized in the pancreas was inversely associated with dynamic measures of b-cell function in non-diabetic men (7). Previous reports described an association of intra-abdominal fat with b-cell function (8,9); however, this was not confirmed by others (10)(11)(12). This seeming discrepancy may be due to the differences in populations studied and the methods by which b-cell function parameters were estimated.…”

“…This seeming discrepancy may be due to the differences in populations studied and the methods by which b-cell function parameters were estimated. In particular, if the magnitude of the insulin secretory response to acute glucose stimulation is used to estimate b-cell function, an association with visceral adipose tissue (VAT) may rather reflect impaired insulin sensitivity (11). Similarly, although liver steatosis is associated with hepatic insulin resistance and inflammation, and was shown to predict T2DM in many different populations (1,2), its relation with b-cell dysfunction is unclear.…”

Orchestration of Glucose Homeostasis

“…As will be discussed below, there is stronger evidence that free fatty acids (FFAs) may play the central role in accounting for the increase in insulin secretory response in the face of nutrient-induced insulin resistance. However, at this moment in time, despite extensive evidence for the hyperbolic relationship between insulin sensitivity and insulin secretion (17,45,59,60), the precise signaling accounting for this fundamental physiological relationship remains unexplained! Needless to say, we continue the search for the mechanism(s) that may explain the "Hyperbolic Law of Glucose Tolerance.…”

Breastfeeding After Gestational Diabetes Pregnancy

“…Thus, lactating women exhibit lower blood glucose and insulin concentrations along with higher rates of glucose production and lipolysis compared with nonlactating women (96). In women with recent GDM, results of a frequently sampled intravenous glucose tolerance test showed that lactating (n ϭ 14) versus nonlactating (n ϭ 12) women had greater ␤-cell compensation for insulin resistance (97). Basal and glucose-stimulated ␤-cell secretory activity in response to a standardized glucose load was lower for lactating women than for nonlactating women (98).…”