Carbohydrate ingestion, with transient endogenous insulinaemia, produces both sympathetic activation and vasodilatation in normal humans

It has been shown that sustained insulin infusion causes an increase in sympathetic vasoconstrictor discharge but, despite this, also causes peripheral vasodilatation. The present study was designed to determine in healthy subjects the effect of ingestion of a carbohydrate meal, with its attendant physiological insulinaemia, on vascular resistance in and sympathetic vasoconstrictor discharge to the same vascular bed, and the relationship between these parameters. Fifteen healthy subjects were studied for 2 h following ingestion of a carbohydrate meal. Calf vascular resistance was measured by venous occlusion plethysmography, and muscle sympathetic nerve activity was assessed by peroneal microneurography. Five of the subjects also ingested water on a separate occasion, as a control. Following the carbohydrate meal, the serum insulin concentration increased to 588+/-72 pmol/l. This was associated with a 47% increase in skeletal muscle blood flow (P<0.001), a 39% fall in vascular resistance (P<0.001) and a 57% increase in sympathetic activity (P<0.001). There was a significant correlation between the increase in insulin and the changes in blood flow, vascular resistance and sympathetic activity. In conclusion, we have shown that ingestion of a carbohydrate meal, with its attendant physiological insulinaemia, was associated with overriding skeletal muscle vasodilatation, despite an increase in sympathetic vasoconstrictor discharge to the same vascular bed. These mechanisms may be important in ensuring optimal glucose uptake and maintenance of blood pressure postprandially

Diabetic hepatosclerosis: another diabetes microvascular complication?

Liver disease in diabetes is common and is frequently the result of hepatic steatosis. Diabetic hepatosclerosis is a relatively recent description of sinusoidal fibrosis, without steatosis, observed in liver biopsies of people with diabetes presenting with cholestasis. Its association with other microvascular complications suggests it is a form of hepatic diabetic microangiopathy.We report the case of a 50-year-old woman with longstanding Type 1 diabetes, complicated by nephropathy resulting in cadaveric renal transplant, retinopathy, gastroparesis and neuropathy with slowly healing ulceration to her right foot. She was noted to have deranged liver function tests: alanine aminotransferase, 162 IU/l; bilirubin, 44 IU/l; alkaline phosphatase, 5279 IU/l (isoenzymes; bone 1029 IU/l, liver 4250 IU/l); γ-glutamyl transferase, 662 IU/l. A non-invasive liver screen did not reveal the cause of the cholestasis. A liver biopsy demonstrated sinusoidal fibrosis without evidence of steatosis and thus a diagnosis of diabetic hepatosclerosis was made. Comparison with a biopsy performed 11 years previously at a different trust due to elevated alkaline phosphatase levels revealed slow progression of the sinusoidal fibrosis.This case describes the longest reported clinical course of diabetic hepatosclerosis, spanning 11 years, in which time the patient did not develop evidence of cirrhosis or portal hypertension. It is difficult to estimate the clinical relevance of this condition because little is known regarding its clinical course and effect on morbidity and mortality. Identified patients should undergo low-intensity, long-term follow-up to improve understanding of its clinical sequelae and relevance