title: Lymphatic system changes in diabetes mellitus: role of insulin and hyperglycemia.
abstract: BACKGROUND
  Diabetic alterations of blood vessels have been well studied, but much less is known about the lymphatic system, which plays an important role in the transport of particles and defensive responses. Accordingly, we investigated lymphatic changes in diabetic rats.
  
  
  METHODS
  Ten, 30 or 60 days after alloxan-induced diabetes (40 mg/kg; i.v.), we studied thoracic duct lymph flow and lymphocyte output, thoracic duct lymph transport of radiotracer particles ((99m)Tc-dextran 500), lymph node uptake and scintigraphic visualization of subcutaneously injected radiotracer particles, as well as the effect of insulin administration and food deprivation.
  
  
  RESULTS
  Diabetes significantly increased thoracic duct lymph flow and the transport of dextran from the footpad subcutaneous tissue. Abnormal lymphocyte output from the thoracic duct occurred in the first 10 days. Uptake of dextran into regional lymph nodes was decreased in diabetes. Insulin per se, although not normalizing blood sugar levels, appeared to recover thoracic duct lymphocyte output and lymph node uptake of (99m)Tc-dextran 500 without affecting the thoracic duct lymph flow or the amount of radiotracer recovered therein. Normalization of glycemia (by food deprivation) restored the lymph flow to control levels without modifying the lymphocyte output. On the other hand, under insulin-restored normoglycemic conditions, both the thoracic duct lymph flow and the lymphocyte output were normalized.
  
  
  CONCLUSIONS
  These findings suggest that variables related to defensive mechanisms, such as lymphocyte recirculation and particles uptake into the lymph nodes can benefit from insulin treatment, whereas glycemic control can benefit transport mechanisms in the lymphatic system, such as lymph flow and lymphatic transport of particles.
authors.affiliation: Department of Pharmacology, Institute of Biomedical Sciences, Universidade de São Paulo, São Paulo, Brasil.
authors.forename: P
authors.initials: P
authors.lastname: Moriguchi
authors.forename: P
authors.initials: P
authors.lastname: Sannomiya
authors.forename: P F
authors.initials: PF
authors.lastname: Lara
authors.forename: R M
authors.initials: RM
authors.lastname: Oliveira-Filho
authors.forename: K V
authors.initials: KV
authors.lastname: Greco
authors.forename: L S
authors.initials: LS
authors.lastname: Sudo-Hayashi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D006943:Hyperglycemia / Q000503:physiopathology*; D007328:Insulin / Q000627:therapeutic use*; D008196:Lymph / Q000502:physiology; D008208:Lymphatic System / Q000503:physiopathology*; D018655:Lymphocyte Count; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D013670:Sodium Pertechnetate Tc 99m / Q000493:pharmacokinetics
chemical_list: D001786:Blood Glucose; D001798:Blood Proteins; D007328:Insulin; D013670:Sodium Pertechnetate Tc 99m