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document
Lack of lipotoxicity effect on { beta } -cell dysfunction in ketosis-prone type 2 diabetes . OBJECTIVE Over half of newly diagnosed obese African Americans with diabetic ketoacidosis ( DKA ) discontinue insulin therapy and go through a period of near-normoglycemia remission . This subtype of diabetes is known as ketosis-prone type 2 diabetes ( KPDM ) . RESEARCH DESIGN AND METHODS To investigate the role of lipotoxicity on beta-cell function , eight obese African Americans with KPDM , eight obese subjects with type 2 diabetes with severe hyperglycemia without ketosis ( ketosis-resistant type 2 diabetes ) , and nine nondiabetic obese control subjects underwent intravenous infusion of 20 % intralipid at 40 ml/h for 48 h. beta-Cell function was assessed by changes in insulin and C-peptide concentration during infusions and by changes in acute insulin response to arginine stimulation ( AIR ( arg ) ) before and after lipid infusion . RESULTS The mean time to discontinue insulin therapy was 11.0 +/- 8.0 weeks in KPDM and 9.6 +/- 2.2 weeks in ketosis-resistant type 2 diabetes ( P = NS ) . At remission , KPDM and ketosis-resistant type 2 diabetes had similar glucose ( 94 +/- 14 vs. 109 +/- 20 mg/dl ) , A1C ( 5.7 +/- 0.4 vs. 6.3 +/- 1.1 % ) , and baseline AIR ( arg ) response ( 34.8 +/- 30 vs. 64 +/- 69 microU/ml ) . P = NS despite a fourfold increase in free fatty acid ( FFA ) levels ( 0.4 +/- 0.3 to 1.8 +/- 1.1 mmol/l , P < 0.01 ) during the 48-h intralipid infusion ; the response to AIR ( arg ) stimulation , as well as changes in insulin and C-peptide levels , were similar among obese patients with KPDM , patients with ketosis-resistant type 2 diabetes , and nondiabetic control subjects . CONCLUSIONS Near-normoglycemia remission in obese African American patients with KPDM and ketosis-resistant type 2 diabetes is associated with a remarkable recovery in basal and stimulated insulin secretion . A high FFA level by intralipid infusion for 48 h was not associated with beta-cell decompensation ( lipotoxicity ) in KPDM patients .
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Intervention_Pharmacological
intravenous infusion of 20 % intralipid at 40 ml/h
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Intervention_Pharmacological
lipid infusion
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Intervention_Pharmacological
intralipid infusion
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Intervention_Pharmacological
intralipid infusion
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Outcome_Physical
{ beta } -cell dysfunction
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Outcome_Physical
beta-cell function
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Outcome_Physical
beta-Cell function
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Outcome_Physical
insulin
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Outcome_Physical
C-peptide concentration
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Outcome_Physical
changes in acute insulin response to arginine stimulation ( AIR ( arg ) )
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Outcome_Physical
mean time to discontinue insulin therapy
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Outcome_Physical
glucose
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Outcome_Physical
baseline AIR ( arg ) response
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Outcome_Physical
free fatty acid ( FFA ) levels
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Outcome_Physical
response to AIR ( arg ) stimulation
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Outcome_Physical
insulin
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Outcome_Physical
C-peptide levels
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Participant_Condition
ketosis-prone type 2 diabetes
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Participant_Condition
obese African Americans with diabetic ketoacidosis ( DKA )
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Participant_Sample-size
eight
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Participant_Condition
obese
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Participant_Condition
KPDM
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Participant_Sample-size
eight
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Participant_Condition
severe hyperglycemia
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Participant_Sample-size
nine
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Participant_Condition
KPDM and ketosis-resistant type 2 diabetes
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Participant_Condition
KPDM