title: Differences in treatment and metabolic abnormalities between normo- and hypertensive patients with type 2 diabetes: the Skaraborg Hypertension and Diabetes Project.
abstract: OBJECTIVE
  To examine treatment and glucose control in type 2 diabetes patients with and without hypertension, and to explore differences in markers for insulin resistance and beta cell function.
  
  
  METHODS
  A community-based, cross-sectional observational study was carried out at the hypertension and diabetes outpatient clinic in primary health care, Skara, Sweden. The subjects were all the 400 patients with type 2 diabetes (202 men, 198 women) who underwent annual follow-up from May 1992 through September 1993; 204 of these also had hypertension.
  
  
  RESULTS
  The patients with both type 2 diabetes and hypertension had a higher b.m.i. (mean; 28.9 kg m(-2) (s.d.; 4.4) vs. 27.4 kg m(-2)(4.6)), higher triglycerides (2.0 mmol l(-1)(1.1) vs. 1.7 mmol l(-1)(1.1)), higher LDL/HDL cholesterol ratio (4.3(1.4) vs. 4.1(1.2)) and higher fasting insulin (8.5 mU l(-1)(1.1) vs. 6.6 mU l(-1)(1.1)). Conversely, glucose levels were lower; HbA1c (6.4%(1.4) vs. 6.8%(1.6)) and fasting blood glucose (8.1 mmol l(-1)(2.3) vs. 8.9 mmol l(-1)(2.7)) than in patients with type 2 diabetes alone. By the homeostasis model assessment (HOMA), patients with type 2 diabetes alone had more impaired beta cell function. They also had a higher frequency of insulin treatment (20% vs. 12%) and were less often treated non-pharmacologically (33% vs. 50%).
  
  
  CONCLUSIONS
  Patients with type 2 diabetes and hypertension constitute a high risk category with a more atherogenic risk factor profile related to the insulin resistance syndrome. Patients with type 2 diabetes without hypertension seem to constitute a subgroup of type 2 diabetes with predominately impaired beta cell function.
authors.affiliation: Department of Community Medicine, Malmö University Hospital, Sweden. ostgren.039010879@telia.com
authors.forename: C J
authors.initials: CJ
authors.lastname: Ostgren
authors.forename: U
authors.initials: U
authors.lastname: Lindblad
authors.forename: E
authors.initials: E
authors.lastname: Bøg-Hansen
authors.forename: J
authors.initials: J
authors.lastname: Ranstam
authors.forename: A
authors.initials: A
authors.lastname: Melander
authors.forename: L
authors.initials: L
authors.lastname: Råstam
mesh_terms: D000368:Aged; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000378:metabolism / Q000628:therapy*; D004032:Diet; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006973:Hypertension / Q000150:complications*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism / Q000627:therapeutic use; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism; D008297:Male; D013548:Sweden; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D014280:Triglycerides