Red blood cell autoantibodies with a shortened erythrocyte life span as a cause of lack of relation between glycosylated hemoglobin and mean blood glucose levels in a woman with type 1 diabetes

Diabetes Care ◽  
1999 ◽  
Vol 22 (12) ◽  
pp. 2085-2086 ◽  
Author(s):  
L. Herranz ◽  
C. Grande ◽  
M. Janez ◽  
F. Pallardo
Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 776-P
Author(s):  
RACHEL BRANDT ◽  
MINSUN PARK ◽  
LAURIE T. QUINN ◽  
MINSEUNG CHU ◽  
YOUNGKWAN SONG ◽  
...  

2020 ◽  
pp. 13-49
Author(s):  
Eileen O'Donnell ◽  
Liam O'Donnell

The diagnosis of Type 1 Diabetes (T1D) will come as an unwelcome surprise to most people. Within a short period of time, the person will have to come to understand and manage this chronic illness. The terminology associated with the T1D condition will also be totally new to the person: diabetes mellitus, pancreas, hyperglycaemia (hyper), hypoglycaemia (hypo), bolus (fast acting insulin), basal (slow acting insulin), ketones and blood glucose levels. The purpose of this article is to assist newly diagnosed patients' understanding of T1D, people who are already living with T1D, carers of people with T1D, partners and family members of someone with T1D, work colleagues, and friends who participate in the same sporting activities or go on holiday with a person who has T1D. In addition, this article reviews how people living with T1D can still enjoy exercise and maintain the best quality of life possible; whilst controlling the blood glucose levels in their body for the rest of their lives to prevent the onset of complications associated with diabetes.


2009 ◽  
Vol 86 (2) ◽  
pp. e31-e33 ◽  
Author(s):  
Daniela Elleri ◽  
Carlo L. Acerini ◽  
Janet M. Allen ◽  
Anne-Mette F. Larsen ◽  
Malgorzata E. Wilinska ◽  
...  

2014 ◽  
Vol 4 (5) ◽  
pp. 20140042 ◽  
Author(s):  
Marie Csete ◽  
John Doyle

Blood glucose levels are controlled by well-known physiological feedback loops: high glucose levels promote insulin release from the pancreas, which in turn stimulates cellular glucose uptake. Low blood glucose levels promote pancreatic glucagon release, stimulating glycogen breakdown to glucose in the liver. In healthy people, this control system is remarkably good at maintaining blood glucose in a tight range despite many perturbations to the system imposed by diet and fasting, exercise, medications and other stressors. Type 1 diabetes mellitus (T1DM) results from loss of the insulin-producing cells of the pancreas, the beta cells. These cells serve as both sensor (of glucose levels) and actuator (insulin/glucagon release) in a control physiological feedback loop. Although the idea of rebuilding this feedback loop seems intuitively easy, considerable control mathematics involving multiple types of control schema were necessary to develop an artificial pancreas that still does not function as well as evolved control mechanisms. Here, we highlight some tools from control engineering used to mimic normal glucose control in an artificial pancreas, and the constraints, trade-offs and clinical consequences inherent in various types of control schemes. T1DM can be viewed as a loss of normal physiologic controls, as can many other disease states. For this reason, we introduce basic concepts of control engineering applicable to understanding pathophysiology of disease and development of physiologically based control strategies for treatment.


2008 ◽  
Vol 23 (3) ◽  
pp. 389-406 ◽  
Author(s):  
Kim Lasecki ◽  
Daniel Olympia ◽  
Elaine Clark ◽  
William Jenson ◽  
Lora Tuesday Heathfield

2012 ◽  
Vol 97 (11) ◽  
pp. 4193-4200 ◽  
Author(s):  
A. J. Fahey ◽  
N. Paramalingam ◽  
R. J. Davey ◽  
E. A. Davis ◽  
T. W. Jones ◽  
...  

Context: Recently we showed that a 10-sec maximal sprint effort performed before or after moderate intensity exercise can prevent early hypoglycemia during recovery in individuals with type 1 diabetes mellitus (T1DM). However, the mechanisms underlying this protective effect of sprinting are still unknown. Objective: The objective of the study was to test the hypothesis that short duration sprinting increases blood glucose levels via a disproportionate increase in glucose rate of appearance (Ra) relative to glucose rate of disappearance (Rd). Subjects and Experimental Design: Eight T1DM participants were subjected to a euglycemic-euinsulinemic clamp and, together with nondiabetic participants, were infused with [6,6-2H]glucose before sprinting for 10 sec and allowed to recover for 2 h. Results: In response to sprinting, blood glucose levels increased by 1.2 ± 0.2 mmol/liter (P < 0.05) within 30 min of recovery in T1DM participants and remained stable afterward, whereas glycemia rose by only 0.40 ± 0.05 mmol/liter in the nondiabetic group. During recovery, glucose Ra did not change in both groups (P > 0.05), but glucose Rd in the nondiabetic and diabetic participants fell rapidly after exercise before returning within 30 min to preexercise levels. After sprinting, the levels of plasma epinephrine, norepinephrine, and GH rose transiently in both experimental groups (P < 0.05). Conclusion: A sprint as short as 10 sec can increase plasma glucose levels in nondiabetic and T1DM individuals, with this rise resulting from a transient decline in glucose Rd rather than from a disproportionate rise in glucose Ra relative to glucose Rd as reported with intense aerobic exercise.


Sign in / Sign up

Export Citation Format

Share Document