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OBJECTIVE -The purpose of this study was to determine whether type 2 diabetic patients have more liver fat than age-, sex-, and BMI-matched nondiabetic subjects and whether liver enzymes (serum alanine aminotransferase [S-ALT] and serum aspartate aminotransferase) are similarly related to liver fat in type 2 diabetic patients and normal subjects. RESEARCH DESIGN AND METHODS -Seventy type 2 diabetic patients and 70nondiabetic subjects matched for BMI, age, and sex were studied. Liver fat ( 1 H-magnetic resonance spectroscopy), body composition (magnetic resonance imaging), and biochemical markers of insulin resistance were measured.RESULTS -The type 2 diabetic patients had, on average, 80% more liver fat and 16% more intra-abdominal fat than the nondiabetic subjects. The difference in liver fat between the two groups remained statistically significant when adjusted for intra-abdominal fat (P Ͻ 0.05). At any given BMI or waist circumference, the type 2 diabetic patients had more liver fat than the nondiabetic subjects. The difference in liver fat between the groups rose as a function of BMI and waist circumference. Fasting serum insulin (r ϭ 0.55, P Ͻ 0.0001), fasting plasma glucose (r ϭ 0.29, P ϭ 0.0006), A1C (r ϭ 0.34, P Ͻ 0.0001), fasting serum triglycerides (r ϭ 0.36, P Ͻ 0.0001), and fasting serum HDL cholesterol (r ϭ Ϫ0.31, P ϭ 0.0002) correlated with liver fat similarly in both groups. The slopes of the relationships between S-ALT and liver fat were significantly different (P ϭ 0.004). Liver fat content did not differ between the groups at low S-ALT concentrations (10 -20 units/l) but was 70 -200% higher in type 2 diabetic patients compared with control subjects at S-ALT concentrations of 50 -200 units/l. CONCLUSIONS -Type 2 diabetic patients have 80% more liver fat than age-, weight-, and sex-matched nondiabetic subjects. S-ALT underestimates liver fat in type 2 diabetic patients. Diabetes Care 31:165-169, 2008I t has been estimated that ϳ70 -80% of type 2 diabetic patients have nonalcoholic fatty liver disease (1,2). In addition, 9 of 12 prospective epidemiological studies have shown that elevated serum liver enzyme concentrations predict type 2 diabetes independent of obesity (3). These data thus suggest that liver fat content is increased in patients with type 2 diabetes compared with equally obese nondiabetic subjects. To date, only one study has addressed this question (4). In this study, liver fat was measured qualitatively using the liver-to-spleen attenuation ratio (4). Liver fat was increased in type 2 diabetic patients compared with 10 weight-matched normal subjects (4). The small number of normal subjects, however, prevents any firm conclusions from being drawn.Clinically, it would be helpful to have a simple measure of liver fat in patients with type 2 diabetes, as liver fat is closely correlated with insulin requirements (5,6) and may be an important parameter to consider when choosing patients for peroxisome proliferator-activated receptor-␥ agonist therapy (7,8). Serum alanine aminotransfera...

OBJECTIVE -Insulin is often postponed for years because initiation is time-consuming. We sought to compare initiation of insulin individually and in groups with respect to change in A1C and several other parameters in type 2 diabetic patients. RESEARCH DESIGN AND METHODS-A randomized (1:1), multicenter, two-arm, parallel design study with a recruiting period of up to 14 weeks and a 24-week treatment period. Either in groups of 4 -8 or individually, using the same personnel and education program, 121 insulin-naive type 2 diabetic patients with an A1C of 7.0 -12.0% were randomized to initiate bedtime insulin glargine. The patients visited the treatment center before and at the time of insulin initiation and at 6, 12, and 24 weeks. Patients self-adjusted the insulin dose to achieve a fasting plasma glucose 4.0 -5.5 mmol/l. RESULTS -At 24 weeks, mean Ϯ SE A1C had decreased from 8.7 Ϯ 0.2 to 6.9 Ϯ 0.1% in those treated individually and from 8.8 Ϯ 0.2 to 6.8 Ϯ 0.1% in those in groups (not significant [NS]). Insulin doses averaged 62 Ϯ 5 IU and 56 Ϯ 5 IU at 24 weeks (NS), respectively. The frequency of hypoglycemia was similar. The total time (visits and phone calls) spent in initiating insulin in the patients in groups (2.2 Ϯ 0.1 h) was 48% less than in those treated individually (4.2 Ϯ 0.2 h). Diabetes treatment satisfaction improved significantly in both sets of patients.CONCLUSIONS -Similar glycemic control and treatment satisfaction can be achieved by initiating insulin in groups and individually. Starting insulin in groups takes one-half as much time as individual initiation.

insulin therapy improves hepatic insulin sensitivity and slightly but significantly reduces liver fat content, independent of serum adiponectin.

Abdominally obese individuals with the metabolic syndrome often have excess fat deposition both intra‐abdominally (IA) and in the liver, but the relative contribution of these two deposits to variation in components of the metabolic syndrome remains unclear. We determined the mutually independent quantitative contributions of IA and liver fat to components of the syndrome, fasting serum (fS) insulin, and liver enzymes and measures of hepatic insulin sensitivity in 356 subjects (mean age 42 years, mean BMI 29.7 kg/m2) in whom liver fat and abdominal fat volumes were measured. IA and liver fat contents were correlated (r = 0.65, P < 0.0001). In multivariate linear regression analyses including either liver or IA fat, liver fat or IA fat explained variation in fS‐triglyceride (TG) and high‐density lipoprotein (HDL) cholesterol, plasma glucose, insulin and liver enzyme concentrations, and hepatic insulin sensitivity independent of age, gender, subcutaneous (SC) fat, and/or lean body mass (LBM). Including both liver and IA fat, liver and IA fat both explained variation in TG, HDL cholesterol, insulin and hepatic insulin sensitivity independent of each other and of age, gender, SC fat, and LBM. Liver fat independently predicted glucose and liver enzymes. SC fat and age explained variation in blood pressure. In conclusion, both IA and liver fat independently of each other explain variation in serum TG, HDL cholesterol, insulin concentrations and hepatic insulin sensitivity, thus supporting that both fat depots are important predictors of these components of the metabolic syndrome.

Background: Liver fat is an important determinant of insulin requirements during insulin therapy. Peroxisome proliferator-activated receptor (PPAR)-␥ agonists reduce liver fat. We therefore hypothesized that type 2 diabetic patients using exceptionally high doses of insulin might respond well to addition of a PPAR␥ agonist.

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Addition of a short-acting insulin secretagogue at main meals improves postprandial hyperglycaemia during combination therapy with basal insulin and metformin, but increases the frequency of hypolycaemia.