Low-dose intraoperative glucose suppressed ketone body production in type 2 diabetes patients under remifentanil anesthesia, but two patients developed hyperglycemia (>11.1 mmol/L), highlighting a tradeoff between metabolic control and blood sugar management. This small RCT raises practical questions about glucose administration during surgery in this population.
Surgical stress and anesthesia create a distinctive metabolic challenge in patients with type 2 diabetes. The body's stress response during surgery triggers glucose production, lipolysis, and ketogenesis as part of the acute phase reaction. This 30-patient randomized controlled trial examined whether providing intraoperative glucose to type 2 diabetes patients anesthetized with remifentanil would alter this metabolic cascade.
The study divided patients into two groups: one receiving no glucose and one receiving a low-dose glucose protocol (0.1 g/kg/h for the first hour, then 0.05 g/kg/h for the second hour). Researchers measured blood glucose, hormones (insulin, cortisol, ACTH), metabolic markers (free fatty acids, ketone bodies), and muscle breakdown indicators (3-methylhistidine) at baseline and multiple timepoints during and after anesthesia.
The glucose-infused group showed the expected result: blood glucose levels rose significantly at 1 and 2 hours post-infusion compared to baseline and the no-glucose group. However, the clinical significance was limited. The free fatty acid levels and markers of muscle protein breakdown (3-methylhistidine/creatinine ratio) did not differ between groups, suggesting that low-dose glucose did not substantially alter lipolysis or proteolysis during surgery. The more nuanced finding involved ketone bodies. Both groups initially showed elevated ketones at 1 hour, reflecting the surgical stress response. But divergence occurred after the 1-hour mark: the no-glucose group maintained elevated ketones, while the low-dose glucose group showed significant suppression of ketogenesis. This is mechanistically consistent with glucose's known role in inhibiting ketone production through insulin signaling.
The hyperglycemia concern materialized modestly but notably: two patients in the low-dose glucose group exceeded 11.1 mmol/L (200 mg/dL), a threshold often considered significant in perioperative glucose management. No patients in the no-glucose group reached this threshold. This small absolute number in a small sample deserves careful interpretation, but it underscores an existing clinical tension: while providing glucose can normalize metabolism in some respects, it carries hyperglycemia risk in insulin-resistant populations undergoing surgery.
This study has limited direct applicability to individuals with type 2 diabetes outside the operating room. The findings are specific to the acute perioperative window under remifentanil anesthesia, a short-acting synthetic opioid used only in hospital settings. If you have type 2 diabetes and require elective surgery, this research suggests a practical consideration for your anesthesia team: low-dose intraoperative glucose may help modulate ketone production during the acute stress response, but it carries modest hyperglycemia risk that requires monitoring. The suppression of ketogenesis itself is neither clearly beneficial nor harmful in the immediate perioperative period, as the study found no corresponding change in free fatty acids or muscle breakdown.
The broader takeaway relates to perioperative glucose management philosophy. Rather than assuming glucose loading universally helps type 2 diabetes patients under stress, individualized approaches that account for baseline glycemic control and insulin sensitivity appear warranted. Discuss your preoperative glucose management plan with your surgical and anesthesia teams, particularly if you take diabetes medications that increase hypoglycemia risk or if your fasting glucose control is suboptimal.
Outside surgery, the metabolic principles shown here (glucose's suppression of ketones, the lipolytic response to surgical stress) are not novel. Blood glucose management and metabolic health in type 2 diabetes remain primarily driven by lifestyle factors: regular physical activity, dietary composition, sleep quality, and weight management. This study refines understanding of acute anesthetic pharmacology rather than offering new interventions for everyday diabetes management.
| Parameter | Details |
|---|---|
| Study type | Randomized controlled trial |
| Sample size | 30 patients with type 2 diabetes |
| Intervention | Low-dose glucose protocol (0.1 g/kg/h x 1 hour, then 0.05 g/kg/h x 1 hour) vs. no glucose during remifentanil anesthesia |
| Primary outcomes | Blood glucose, ketone bodies, free fatty acids, 3-methylhistidine/creatinine ratio, hormonal markers (insulin, cortisol, ACTH) |
| Key finding | Low-dose glucose suppressed ketogenesis but elevated blood glucose in 2/15 patients above 11.1 mmol/L |
| Journal | The Journal of Medical Investigation |
| Publication date | February 2026 |
| PubMed ID | 42021080 |
Alotaibi, et al. Effect of glucose load on metabolism in patients with type 2 diabetes during elective surgery using remifentanil-induced anesthesia: a randomized controlled trial. *The Journal of Medical Investigation*. 2026;73:222-228. PubMed: 42021080
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