Given a passage, 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.

Ex Input:
Increased lipid supply causes beta cell death, which may contribute to reduced beta cell mass in type 2 diabetes. We investigated whether endoplasmic reticulum (ER) stress is necessary for lipid-induced apoptosis in beta cells and also whether ER stress is present in islets of an animal model of diabetes and of humans with type 2 diabetes.', 'Expression of genes involved in ER stress was evaluated in insulin-secreting MIN6 cells exposed to elevated lipids, in islets isolated from db/db mice and in pancreas sections of humans with type 2 diabetes. Overproduction of the ER chaperone heat shock 70 kDa protein 5 (HSPA5, previously known as immunoglobulin heavy chain binding protein [BIP]) was performed to assess whether attenuation of ER stress affected lipid-induced apoptosis.', 'We demonstrated that the pro-apoptotic fatty acid palmitate triggers a comprehensive ER stress response in MIN6 cells, which was virtually absent using non-apoptotic fatty acid oleate. Time-dependent increases in mRNA levels for activating transcription factor 4 (Atf4), DNA-damage inducible transcript 3 (Ddit3, previously known as C/EBP homologous protein [Chop]) and DnaJ homologue (HSP40) C3 (Dnajc3, previously known as p58) correlated with increased apoptosis in palmitate- but not in oleate-treated MIN6 cells. Attenuation of ER stress by overproduction of HSPA5 in MIN6 cells significantly protected against lipid-induced apoptosis. In islets of db/db mice, a variety of marker genes of ER stress were also upregulated. Increased processing (activation) of X-box binding protein 1 (Xbp1) mRNA was also observed, confirming the existence of ER stress. Finally, we observed increased islet protein production of HSPA5, DDIT3, DNAJC3 and BCL2-associated X protein in human pancreas sections of type 2 diabetes subjects.

Ex Output:
Does endoplasmic reticulum stress contribute to beta cell apoptosis in type 2 diabetes?

Ex Input:
To describe the prevalence of prolonged fatigue, chronic fatigue syndrome (CFS)-like illness, and associated symptom patterns in adolescents attending primary care.', 'The design was cross-sectional. A questionnaire designed by the authors assessing fatigue and associated symptoms was administered to 901 adolescents (aged 11-18 years) attending 12 primary care clinics in the Chicago area. Prevalence rates for prolonged fatigue and CFS-like illness were calculated. Univariate comparisons involving sociodemographic data and fatigue severity were made between adolescents with and without prolonged fatigue, and sociodemographic and symptom predictors of prolonged fatigue were identified using logistic regression analysis.', 'Prolonged fatigue (> or = 1 month) occurred at a rate of 8.0% and CFS-like illness occurred at a rate of 4.4%. Adolescents with prolonged fatigue were significantly older and also reported greater fatigue severity than those without fatigue. Findings from logistic regression indicated that, in addition to increasing age, headaches, muscle pains, fever, and fatigue made worse by exercise were significantly associated with prolonged fatigue.

Ex Output:
Does sociodemographic and symptom correlate of fatigue in an adolescent primary care sample?

Ex Input:
Fructose may play a crucial role in the pathogenesis of metabolic syndrome (MetS). However, the pathogenic mechanism of the fructose-induced MetS has not yet been investigated fully. Recently, several reports have investigated the association between mitochondrial DNA (mtDNA) and MetS. We examined the effect of fructose-rich diets on mtDNA content, transcription, and epigenetic changes.', 'Four-week-old male Sprague-Dawley rats were offered a 20% fructose solution for 14weeks. We quantified mRNAs for hepatic mitochondrial genes and analyzed the mtDNA methylation (5-mC and 5-hmC) levels using ELISA kits.', 'Histological analysis revealed non-alcoholic fatty liver disease (NAFLD) in fructose-fed rats. Hepatic mtDNA content and transcription were higher in fructose-fed rats than in the control group. Global hypomethylation of mtDNA was also observed in fructose-fed rats.

Ex Output:
Does fructose consumption induce hypomethylation of hepatic mitochondrial DNA in rats?