The relation of diabetic control to in vivo pH of soft tissue abscesses

A N Bessman1, P J Geiger, L J Thomas

  • 1Department of Medicine, Rancho Los Amigos-University of Southern California Medical Center, Downey.

Biochemical Medicine and Metabolic Biology
|October 1, 1990
PubMed

Insights

Diabetic mice with induced soft tissue abscesses show lower intra-abscess pH, indicating altered white cell metabolism. Insulin treatment in diabetic mice improved pH towards normal levels, suggesting an in vivo effect on white cell activity.

Area of Science:

  • Infectious Diseases
  • Endocrinology
  • Immunology

Background:

  • Uncontrolled diabetes is associated with impaired host defense mechanisms.
  • Previous studies suggest lower intra-abscess pH in diabetic hosts, potentially due to altered white blood cell (WBC) metabolism.

Purpose of the Study:

  • To compare intra-abscess pH in nondiabetic, untreated diabetic, and insulin-treated diabetic mice.
  • To investigate the in vivo effect of insulin on WBC activity within abscesses.

Main Methods:

  • Induced soft tissue abscesses in three groups of mice: nondiabetic, untreated diabetic, and insulin-treated diabetic.
  • Diabetes was induced using streptozotocin; abscesses were infected with B. fragilis and Enterococcus.
  • Measured blood glucose, peritoneal pH, intra-abscess pH, and bacterial colony counts.

Main Results:

  • Intra-abscess pH was significantly lower in untreated diabetic mice (6.85) and insulin-treated diabetic mice (6.08) compared to nondiabetic controls (6.97).
  • Blood glucose levels were significantly higher in untreated (256 mg%) and insulin-treated (712.8 mg%) diabetic mice compared to nondiabetic controls (189 mg%).
  • Insulin treatment showed a trend towards normalizing intra-abscess pH but resulted in a wider range of values.

Conclusions:

  • Diabetic status significantly impacts intra-abscess pH, likely reflecting altered WBC function.
  • This study provides evidence for an in vivo effect of insulin on WBC activity in the context of infection.

Related Concept Videos

Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Diabetic Foot Ulcer01:31

Diabetic Foot Ulcer

Definition A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.Pathophysiology • The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing. • Neuropathy is the most common factor. Sensory neuropathy reduces pain perception,...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...