Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Input: Consider Input: Context: Normal glucose metabolism depends on pancreatic secretion of insulin and glucagon. The bihormonal hypothesis states that while lack of insulin leads to glucose underutilisation, glucagon excess is the principal factor in diabetic glucose overproduction. A recent study reported that streptozotocin-treated glucagon receptor knockout mice have normal glucose tolerance. We investigated the impact of acute disruption of glucagon secretin or action in a mouse model of severe diabetes by three different approaches: (1) alpha cell elimination; (2) glucagon immunoneutralisation; and (3) glucagon receptor antagonism, in order to evaluate the effect of these on glucose tolerance.', 'Severe diabetes was induced in transgenic and wild-type mice by streptozotocin. Glucose metabolism was investigated using OGTT in transgenic mice with the human diphtheria toxin receptor expressed in proglucagon producing cells allowing for diphtheria toxin (DT)-induced alpha cell ablation and in mice treated with either a specific high affinity glucagon antibody or a specific glucagon receptor antagonist.', 'Near-total alpha cell elimination was induced in transgenic mice upon DT administration and resulted in a massive decrease in pancreatic glucagon content. Oral glucose tolerance in diabetic mice was neither affected by glucagon immunoneutralisation, glucagon receptor antagonism, nor alpha cell removal, but did not deteriorate further compared with mice with intact alpha cell mass.
Answer: Disruption of glucagon action/secretion did not improve glucose tolerance in diabetic mice. Near-total alpha cell elimination may have prevented further deterioration. Our findings support insulin lack as the major factor underlying hyperglycaemia in beta cell-deficient diabetes.

Output: Does acute disruption of glucagon secretion or action improve glucose tolerance in an insulin-deficient mouse model of diabetes?


Input: Consider Input: Context: Blood oxygen level-dependent (BOLD) MRI has been effectively used to monitor changes in renal oxygenation. However, R2* (or T2*) is not specific to blood oxygenation and is dependent on other factors. This study investigates the use of a statistical model that takes these factors into account and maps BOLD MRI measurements to blood pO2.', "Spin echo and gradient echo images were obtained in six Sprague-Dawley rats and R2 and R2* maps were computed. Measurements were made at baseline, post-nitric oxide synthase inhibitor (L-NAME), and post-furosemide administration. A simulation of each region was performed to map R2' (computed as R2*-R2) to blood pO2.", 'At baseline, blood pO2 in the outer medulla was 30.5\u2009±\u20091.2 mmHg and 51.9\u2009±\u20095.2 mmHg in the cortex, in agreement with previous invasive studies. Blood pO2 was found to decrease within the outer medulla following L-NAME (P\u2009<\u20090.05) and increase after furosemide (P\u2009<\u20090.05). Blood pO2 in the cortex increased following furosemide (P\u2009<\u20090.05).
Answer: Model-derived blood pO2 is sensitive to pharmacological challenges, and baseline pO2 is comparable to literature values. Reporting pO2 instead of R2* could lead to a greater clinical impact of renal BOLD MRI and facilitate the identification of hypoxic regions. Magn Reson Med, 2016. © 2016 International Society for Magnetic Resonance in Medicine.

Output: Is bOLD quantified renal pO2 sensitive to pharmacological challenges in rats?


Input: Consider Input: Context: To discriminate non-proliferative diabetic retinopathy (NPDR) patients from healthy controls by fluorescence lifetime imaging ophthalmoscopy (FLIO).', 'A prototype FLIO (Heidelberg-Engineering, Heidelberg, Germany) was used to examine the retina of 33 patients and 28 controls. As increased fluorescence of the diabetic lens is known, the lenses of 34 patients and 24 controls were investigated as well. Time-resolved decay was detected in two spectral channels (ch1: 498-560\xa0nm, ch2: 560-720\xa0nm) and approximated by a series of three exponential functions yielding in lifetimes (τ', 'Significant differences between patients and controls were found for all fundus lifetime components (τ
Answer: Fundus Fluorescence lifetimes are significantly increased in NPDR while lens lifetimes are shorter in the patient group. Lifetime changes might be indicative for the accumulation of advanced glycation end products (AGEs) which enables detection of the disease with high sensitivity and specificity possibly bearing diagnostic merit.


Output: Are fundus autofluorescence lifetimes increased in non-proliferative diabetic retinopathy?