1,721,226 research outputs found
Alterations of glucose metabolism in type 2 diabetes mellitus. An overview.
No full textThe main pathogenetic mechanisms responsible for hyperglycemia in type 2 diabetes mellitus are reviewed
In vivo metabolic defects in non-insulin-dependent diabetes mellitus
No full textIn 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 homoeostasi
Plasma glucose levels throughout the day and HbA1c interrelationships in type 2 diabetes. Implications for treatment and monitoring of metabolic control
No full textRole of reduced β-cell mass versus impaired β-cell function in the pathogenesis of type 2 diabetes
No full textNot Presen
Glucose metabolism in obesity and type 2 diabetes
No full textThe aim of this review is to provide a comprehensive summary of the subject of
glucose metabolism in normal and obese subjects, and in those with type 2
diabetes. The following topics are discussed: Glucose and insulin metabolism,
including characterization of the role of various organs in maintaining glucose
homeostasis in the basal state and after food. The action of insulin and the
concept of insulin resistance, its main characteristics as revealed by studies of
glucose metabolism in liver and skeletal muscle, the two organs primarily
involved. Changes in insulin secretion in obese subjects and in diabetics are
reviewed. Finally, the development of diabetes as a consequence of increasing
insulin resistance in the obese diabetic subject is discussed. The principal
features--insulin resistance, elevated free fatty acid levels and
glucotoxicity--are emphasized. A possible explanation of how obesity leads to
diabetes, emphasizing the role played by upper body fat distribution, is
provided
Glucose and free fatty acid metabolism in human obesity. Relationship with insulin resistance
No full text
A Novel Insulin/Glucose Model after a Mixed-Meal Test in Patients with Type 1 Diabetes on Insulin Pump Therapy
Full text linkCurrent closed-loop insulin delivery methods stem from sophisticated models of the glucose-insulin (G/I) system, mostly based on complex studies employing glucose tracer technology. We tested the performance of a new minimal model (GLUKINSLOOP 2.0) of the G/I system to characterize the glucose and insulin dynamics during multiple mixed meal tests (MMT) of different sizes in patients with type 1 diabetes (T1D) on insulin pump therapy (continuous subcutaneous insulin infusion, CSII). The GLUKINSLOOP 2.0 identified the G/I system, provided a close fit of the G/I time-courses and showed acceptable reproducibility of the G/I system parameters in repeated studies of identical and double-sized MMTs. This model can provide a fairly good and reproducible description of the G/I system in T1D patients on CSII, and it may be applied to create a bank of "virtual" patients. Our results might be relevant at improving the architecture of upcoming closed-loop CSII systems
Treatment intensification in patients with inadequate glycemic control on basal insulin: Rationale and clinical evidence for the use of short-acting and other glucagon-like peptide-1 receptor agonists
Full text linkA substantial proportion of patients with type 2 diabetes mellitus do not reach glycemic targets, despite treatment with oral anti-diabetic drugs and basal insulin therapy. Several options exist for treatment intensification beyond basal insulin, and the treatment paradigm is complex. In this review, the options for treatment intensification will be explored, focusing on drug classes that act via the incretin system and paying particular attention to the short-acting glucagon-like peptide-1 receptor agonists exenatide and lixisenatide. Current treatment guidelines will be summarized and discussed
Role of free fatty acids and insulin in determining free fatty acid and lipid oxidation in man
No full textPlasma FFA oxidation (measured by infusion of 14C-palmitate) and net lipid
oxidation (indirect calorimetry) are both inhibited by insulin. The present study
was designed to examine whether these insulin-mediated effects on lipid
metabolism resulted from a decline in circulating FFA levels or from a direct
action of the hormone on FFA/lipid oxidation. Nine subjects participated in two
euglycemic insulin clamps, performed with and without heparin. During each
insulin clamp study insulin was infused at two rates, 4 and 20 mU/m2.min for 120
min. The studies were performed with indirect calorimetry and 3-3H-glucose and
14C-palmitate infusion. During the control study plasma FFA fell from 610 +/- 46
to 232 +/- 42 to 154 +/- 27 mumol/liter, respectively. When heparin was infused
basal plasma FFA concentration remained constant. During the control study,
FFA/lipid oxidation rates decreased in parallel with the fall in the plasma FFA
concentration. During the insulin/heparin study, plasma 14C-FFA oxidation
remained unchanged while net lipid oxidation decreased. In conclusion, when the
plasma FFA concentration is maintained unchanged by heparin infusion, insulin has
no direct effect on FFA turnover and disposal. These results thus suggest that
plasma FFA oxidation is primarily determined by the plasma FFA concentration,
while net lipid oxidation is regulated by both the plasma FFA and the insulin
level
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