Onesmo Balemba

My research focuses on the pathophysiology of diseases that affect gastrointestinal (GI) functions. My aim is to gain a better understanding of neuromuscular and immune system host responses in diabetes, and infectious diarrhea, and therapeutic strategies for these conditions.

My research focuses on the pathophysiology of diseases that affect gastrointestinal (GI) functions. My aim is to gain a better understanding of neuromuscular and immune system host responses in diabetes, and infectious diarrhea, and therapeutic strategies for these conditions.

• Anti-diarrhea remedy
  Diarrheal diseases are among the leading causes of illness and death of children and HIV/AIDS patients and a major symptom of stress. There is wide range of the causative agents, and cellular mechanisms leading to the development of the symptoms of diarrhea are complexity and diverse. Therefore, the effective treatment of diarrheal diseases requires more than one drug in order to alleviate the symptoms of increased motility, secretion and abdominal pain; to eliminate the etiological agent(s) and to treat the associated inflammation. There is need for new therapeutic agents especially drugs that reduce enteric neurotransmission, which is the main factor underlying increased bowel movements and abdominal discomfort/pain.
  
  Herbal extracts have been used for thousands of years to treat diarrhea, and still are widely used to treat diarrheal diseases. We are investigating the efficacy of extracts from the bark of Garcinia buchananii as anti-diarrheal folk remedy of diarrheal disease, anti-inflammatory, and analgesic activities effects. The long-term goal is to conduct thorough scientific investigations of the efficacy and safety of the extracts; isolate the bioactive components; and determine cellular mechanisms underlying actions related to anti-diarrhea, pain and inflammatory activity; and promote the use of extracts as an affordable natural herbal drug to treat diarrhea and associated pain and inflammation.
• Obesity & Type 2 Diabetes Mellitus
  Obesity and type 2 diabetes mellitus studies in a mouse model
  Obesity and T2DM are metabolic diseases of major socioeconomic impact, morbidity and mortality. Worldwide, about one in every 10 adults are overweight and roughly 150 million people have T2DM. The risk factors for developing T2DM include: overweight, inactivity, genetic predisposition (family history and race) as well as aging. Cardinal features of T2DM are: obesity, insulin resistance, glucose intolerance, and low grade inflammation. Disease events originate in the gastrointestinal (GI) tract, and GI organs are a prime target for successful therapeutic intervention against obesity and T2DM. Recent studies indicate that the interaction between excessive calories and microorganisms in the GI tract, disrupted mucosal permeability, and chylomicron-mediated lipopolysaccharide (LPS) trans-epithelial transport causes endotoxemia. The latter induces fat deposition, inflammation and insulin resistance, the metabolic syndromes that ultimately develop into obesity and T2DM.
  
  Diabetic neuronal cell death and altered neurochemistry (neuropathy) occur in the enteric nervous system (ENS; the “little brain” in the gut) because it is morphologically and functionally similar to the brain) of humans and experimental animals. Neuropathy is considered to be a key factor underlying bowel disorders that are common among obese and T2DM patients New research data indicate that enteric neural mechanisms have a crucial role in the development and in the therapeutic interventions against obesity and T2DM. The role of the ENS in the pathophysiology of obesity and T2DM is not fully understood. The first long-term goal of our research program is to gain a better understanding of how excessive caloric intake, especially the consumption of fatty acids disrupts neurotransmission, and causes injury and death of enteric neurons. The second goal of this research is to utilize anti-inflammatory neural mechanisms to protect the ENS and preserve mucosal-barrier function, thus controlling the metabolic endotoxemia. These investigations will enhance understanding of the pathogenesis of GI motility disorders that are widespread in type 2 diabetics and shed light on how the enteric neuromuscular axis can be protected from damages induced by excessive calories and subsequent metabolic syndromes. These breakthroughs will contribute to the development of effective treatments of neurological disorders, improving quality of life of obese and T2DM patients.