Excessive carbohydrate intake increases the risk of obesity and type 2 diabetes and worsens glycemic control in diabetic patients. We conducted a randomized, single-blind, placebo-controlled trial in 19 healthy adults to compare the glycolipid metabolism effects of eating low-carbohydrate cake (carbohydrate content except erythritol and fiber: <5 g per 100 g) to those from eating regular-carbohydrate cake. Although there was no significant differences in the primary endpoint of blood glucose levels at 60 minutes after eating, the secondary endpoints of blood glucose and insulin levels at 30 minutes after eating, incremental area under the curve, and maximum concentration were all significantly lower in the low-carbohydrate cake group than in the regular-carbohydrate cake group. The active glucagon-like peptide-1 (GLP-1) level was significantly higher in the low-carbohydrate cake group than in the regular-carbohydrate cake group at 60 minutes postprandially, and free fatty acids were higher in the low-carbohydrate cake group than in the regular-carbohydrate cake group at 90 minutes postprandially but were not markedly increased compared with the preprandial levels. There were no marked differences in the triglyceride, remnant-like particle cholesterol (RLP-C), or ApoB-48 levels. In conclusion, intake of low-carbohydrate cake suppressed postprandial blood glucose elevation and increased the concentration of active GLP-1 in healthy subjects. The health effects of long-term consumption of low-carbohydrate cake remain to be determined.

The patient was a 58-year-old woman with type 2 diabetes and obesity medicated by an SGLT2 inhibitor and biguanide. She had no medical history of diabetic ketoacidosis. She visited our emergency room with upper abdominal pain, vomiting, and diarrhea for four days despite discontinuing all oral hypoglycemic agents. Emergency upper gastrointestinal endoscopy revealed acute duodenitis. Blood and urine tests revealed that her blood glucose level was 211 mg/dL, HbA1c 8.2 %, urine ketone bodies (3+), and venous blood gas pH 7.291, indicating euglycemic DKA during treatment with an SGLT2 inhibitor. As both islet-related and thyroid-related auto-antibodies were positive, she was finally diagnosed with SPIDDM with Graves' disease. In this case, euglycemic DKA seems to have been caused by four factors: insufficient carbohydrate intake due to acute duodenitis, potential insulin insufficiencies due to SPIDDM, accelerated fat catabolism due to hyperthyroidism, and oral intake of an SGLT2 inhibitor.