In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[EX Q]: Context: Approximately 50% of subjects with essential hypertension (EH) are insulin resistant, and this defect in insulin action could contribute to increased cardiovascular disease (CVD) risk in these patients. To test this hypothesis, we attempted to see if there was a link between insulin resistance (IR) and carotid intimal medial thickness (IMT), an early index of CVD, in patients with essential hypertension.', 'Ultrasound quantification of carotid IMT was performed in 79 hypertensive patients, and 63 patients (31 m and 32 f), defined as being free of plaque (IMT < 1.3 mm), were further subdivided into normal (<1.0 mm) and thickened (1-1.3 mm) IMT groups. Subjects in the thickened IMT group were older and had significantly (p < 0.05) higher plasma concentrations of fasting insulin, nitric oxide (NO(x)) and intercellular adhesion molecule 1 (ICAM-1). However, the two groups were not significantly different in terms of blood pressure, overall or regional obesity, fasting lipid levels, uric acid, concentrations of other cellular adhesion molecules or levels of C-reactive protein. There were significant (p < 0.05) correlations in the whole population between IMT and age, fasting insulin and NO(x), and multiple regression analysis identified fasting insulin as an independent predictor of IMT.\Question: Do insulin resistance/compensatory hyperinsulinemia predict carotid intimal medial thickness in patients with essential hypertension?
[EX A]: The presence of increased IMT is significantly related to several metabolic and endothelial abnormalities associated with IR/hyperinsulinemia, and fasting insulin independently predicts the thickness of the intima-media layer. These results support the view that CVD risk is greatest in those patients with essential hypertension who are also IR/hyperinsulinemic.

[EX Q]: Context: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction.', "Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as mean\u2009±\u2009SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey's post hoc test.", 'Creatinine clearance (μL/min) was similar between C57 (171\u2009±\u200917) and ApoE (140\u2009±\u200926) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112\u2009±\u20098, ~\u2009-\u200935%, p\u2009<\u20090.05) and ApoE (61\u2009±\u200910, ~\u2009-\u200956%, p\u2009<\u20090.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73\u2009±\u20097; OVX: 73\u2009±\u20098, p\u2009<\u20090.05) when compared to C57 animals (Sham: 49\u2009±\u20093; OVX: 60\u2009±\u20094), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1\u2009±\u20095.7; OVX: 33.7\u2009±\u20094.7) and ApoE sham animals (26.4\u2009±\u20093.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6\u2009±\u20095.8, p\u2009<\u20090.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.2\u2009±\u20090.4; C57 OVX: 22.9\u2009±\u20091.0; ApoE Sham: 13.9\u2009±\u20090.7; ApoE OVX: 34.0\u2009±\u20091.4 au x 103, p\u2009<\u20090.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0\u2009±\u20090; C57 OVX: 0\u2009±\u20090; ApoE Sham: 6.8\u2009±\u20091.6; ApoE OVX: 5.2\u2009±\u20090.8% x 10-2, p\u2009<\u20090.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78\u2009±\u20090.04; ApoE: 0.81\u2009±\u20090.04 au, p\u2009<\u20090.05) when compared to sham animals (C57:1.00\u2009±\u20090.04; ApoE: 1.03\u2009±\u20090.03 au).\Question: Do endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice?
[EX A]: Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women.

[EX Q]: Context: Guanylin activates an intestinal guanylate cyclase (GCC) and stimulates electrolyte movement across the gut epithelium. Cells expressing guanylin messenger RNA have been localized to the epithelial cell layer of the intestine; however, the identity of the guanylin-producing cells has not been determined. The aim of this study was to identify cells that express guanylin in the rat intestine.', 'Antibodies were raised against defined proguanylin epitopes, evaluated by Western blotting, and used for immunoperoxidase histochemistry.', 'Guanylin-like immunoreactivity was localized to a subset of goblet cells. In the small intestine, most, perhaps all, goblet cells in the villi were immunopositive, as were some goblet cells in upper crypts; however, goblet cells deep within crypts were unlabeled. In the colon, goblet cells clustered in the necks and around the openings of crypts were immunopositive, whereas (as in the small intestine) goblet cells in deeper crypt regions were unlabeled. In some animals, immunoreactive columnar epithelial cells were also observed in the colon (although such cells were not apparent in the small intestine). Relative labeling of columnar cells varied from animal to animal.\Question: Is guanylin , an endogenous ligand for C-type guanylate cyclase , produced by goblet cells in the rat intestine?
[EX A]:
Guanylin is expressed in mature goblet cells. If secreted in conjunction with mucin, it could play a role in the hydration of mucus.