In patients with non-insulin-dependent diabetes mellitus (NIDDM) alterations in insulin secretion and insulin action coexist, and create and sustain hyperglycaemia, which results from an imbalance between glucose production and glucose utilization. The target organs for insulin action are the liver (restriction of glucose production), the muscle (acceleration of glucose disposal) and the adipose tissue (inhibition of free fatty acid mobilization). In NIDDM, the liver produces an inordinate amount of glucose, secondary to an acceleration of gluconeogenesis, and is insensitive to the inhibitory action of insulin on glucose production. In NIDDM, skeletal muscle takes up less glucose in response to hyperinsulinaemia. Adipose tissue mobilizes a larger amount of free fatty acid, thereby possibly enhancing glucose production in the liver (Randle's cycle of metabolic competition between free fatty acids and glucose). Thus, the in vivo assessment of insulin action in NIDDM reveals a web of possibly interrelated metabolic defects, which in association with impaired insulin secretion cause a permanent, profound disruption of glucose homoeostasis

In vivo metabolic defects in non-insulin-dependent diabetes mellitus

BONADONNA, Riccardo
1993

Abstract

In patients with non-insulin-dependent diabetes mellitus (NIDDM) alterations in insulin secretion and insulin action coexist, and create and sustain hyperglycaemia, which results from an imbalance between glucose production and glucose utilization. The target organs for insulin action are the liver (restriction of glucose production), the muscle (acceleration of glucose disposal) and the adipose tissue (inhibition of free fatty acid mobilization). In NIDDM, the liver produces an inordinate amount of glucose, secondary to an acceleration of gluconeogenesis, and is insensitive to the inhibitory action of insulin on glucose production. In NIDDM, skeletal muscle takes up less glucose in response to hyperinsulinaemia. Adipose tissue mobilizes a larger amount of free fatty acid, thereby possibly enhancing glucose production in the liver (Randle's cycle of metabolic competition between free fatty acids and glucose). Thus, the in vivo assessment of insulin action in NIDDM reveals a web of possibly interrelated metabolic defects, which in association with impaired insulin secretion cause a permanent, profound disruption of glucose homoeostasis
"insulin resistance; type 2 diabetes; insulin secretion"
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11562/434900
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