DAY-TO-DAY VARIATIONS IN FASTING PLASMA GLUCOSE AND FASTING PLASMA INSULIN LEVELS IN LATE NORMAL PREGNANCY

Author(s):  
D. M. Campbell ◽  
P. D. Bewsher ◽  
J. M. Davidson ◽  
H. W. Sutherland
2019 ◽  
Author(s):  
Lingyun Ma ◽  
Daohuang Luo ◽  
Ting Yang ◽  
Songtao Wu ◽  
Min Li ◽  
...  

Abstract Background: Acromegaly is a rare, chronic and severe disease . Drug therapy including somatostatin analogues , dopamine receptor agonists and growth hormone receptor antagonists are commonly used to treat patients who do not responde to surgery. T he use of combination therapy with PEG and SAs has become more common over the last decade . We performed this study t o accurately evaluate the effect of combination therapy of somatostatin analogues (SAs) with pegvisomant (PEG) on acromegalic patients. Methods: PubMed, EMBASE, The Cochrane Library, and ClinicalTrials.gov were searched for relevant studies. Prospective clinical trials treating acromegaly with the co-administration of SAs and PEG were included. We performed a meta-analysis by using Stata 12.1 . Sensitivity analysis was conducted to explore heterogeneity. Results: Eight studies were included in this meta-analysis. The overall rate of serum insulin-like growth factor 1 (IGF-1) normalization was 75% (95% CI: 50%–93%; I 2 =93.60%). The combination therapy did not significantly change patients’ fasting plasma glucose (ES: 0.011 mmol*L -1 ; 95% CI: − 0.374 to 0.397 mmol*L -1 ; P=0.954) or glycosylated haemoglobin (ES: -0.106%; 95% CI: − 0.302% to 0.089%; P=0.285) while decreasing the fasting plasma insulin (ES: −21.487 pmol*L-1; 95% CI: −35.713 to -7.260 pmol*L-1; P=0.003). Elevation of liver enzyme levels was found in 14% (95% CI: 10% to 19%) of the patients. Conclusions: Combined therapy of SAs and PEG effectively normalized IGF-1 levels in most of the patients whose IGF-1 level was greater than the upper limit of normal after high dose SAs monotherapy. The combination therapy significantly decreased patients’ fasting plasma insulin. However, improved fasting plasma glucose or glycosylated haemoglobin was not found during the combination therapy. Moreover, elevated liver enzyme levels were observed in a small number of patients, which suggests a need for liver function monitoring. Trial registration We have our protocol registered in PROSPERO. (Registration number: CRD42019115549)


1987 ◽  
Vol 72 (1) ◽  
pp. 135-138 ◽  
Author(s):  
Kenneth F. Whyte ◽  
George J. Addis ◽  
Robert Whitesmith ◽  
John L. Reid

1. Regulation of magnesium balance is poorly understood. However, hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infarction, cardiac surgery and insulin-induced hypoglycaemia stress tests. 2. The effects of l-adrenaline infusions, sufficient to achieve pathophysiological levels of adrenaline, and of therapeutic intravenous infusions of salbutamol, a β2-agonist, on plasma magnesium, plasma potassium, plasma glucose and plasma insulin levels were studied in a placebo-controlled design in eight normal subjects. 3. Plasma magnesium levels fell significantly during the adrenaline infusion and also during the salbutamol infusion, though more slowly. In a 1 h period of observation after cessation of the infusions no recovery of plasma magnesium levels was seen. Significant falls in plasma potassium levels were also observed during both infusions with spontaneous recovery within 30 min after the infusions. 4. No significant changes in plasma insulin levels occurred with either salbutamol or l-adrenaline compared with control. Plasma glucose levels rose significantly during the adrenaline infusion. 5. The study suggests that both l-adrenaline and salbutamol cause shifts in plasma magnesium which are not mediated by insulin. We propose that intracellular shifts of magnesium occur as a result of β-adrenergic stimulation.


2011 ◽  
Vol 96 (6) ◽  
pp. 1763-1770 ◽  
Author(s):  
E. Cersosimo ◽  
A. Gastaldelli ◽  
A. Cervera ◽  
E. Wajcberg ◽  
A. Sriwijilkamol ◽  
...  

Objective: Our objective was to examine the mechanisms via which exenatide attenuates postprandial hyperglycemia in type 2 diabetes mellitus (T2DM). Study Design: Seventeen T2DM patients (44 yr; seven females, 10 males; body mass index = 33.6 kg/m2; glycosylated hemoglobin = 7.9%) received a mixed meal followed for 6 h with double-tracer technique ([1-14C]glucose orally; [3-3H]glucose iv) before and after 2 wk of exenatide. In protocol II (n = 5), but not in protocol I (n = 12), exenatide was given in the morning of the repeat meal. Total and oral glucose appearance rates (RaT and RaO, respectively), endogenous glucose production (EGP), splanchnic glucose uptake (75 g − RaO), and hepatic insulin resistance (basal EGP × fasting plasma insulin) were determined. Results: After 2 wk of exenatide (protocol I), fasting plasma glucose decreased (from 10.2 to 7.6 mm) and mean postmeal plasma glucose decreased (from 13.2 to 11.3 mm) (P < 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.9 to 10.8 μmol/kg · min, P < 0.05), and hepatic insulin resistance declined (both P < 0.05). RaO, gastric emptying (acetaminophen area under the curve), and splanchnic glucose uptake did not change. In protocol II (exenatide given before repeat meal), fasting plasma glucose decreased (from 11.1 to 8.9 mm) and mean postmeal plasma glucose decreased (from 14.2 to 10.1 mm) (P < 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.4 to 10.7 μmol/kg · min, P = 0.05). RaT and RaO decreased markedly from 0–180 min after meal ingestion, consistent with exenatide's action to delay gastric emptying. Conclusions: Exenatide improves 1) fasting hyperglycemia by reducing basal EGP and 2) postmeal hyperglycemia by reducing the appearance of oral glucose in the systemic circulation.


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